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Pathophysiology Final Exam Review

Pathophysiology (Nova Southeastern University)

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PATHO FINAL (100 Q’s)


1. Differences b/w dysplasia, hyperplasia, physiological (6 q)
a. Dysplasia = deranged growth immature cells of a specific tissue that
results in atypical cells (cells vary in size, shape, and appearance)
i. often a precursor of cancer (ex. cervical dysplasia – cells start to
change + become precancerous or cancerous)
ii. * Google: Dysplasia refers to an abnormality in the maturation of
cells within a tissue; consists of an increase in immature cells with
a corresponding decrease in mature cells. Dysplasia is often
indicative of an early neoplastic process (neoplasia is the process
underlying cancer and some benign tumors)
b. Hyperplasia = increase in the # of cells in an organ or tissue
i. an organ can get enlarged as a result
ii. normal cells but there are more in number compared to normal human
body
iii. CONTROLLED process that occurs in response to an appropriate
stimulus (could be physiologic or non) and goes away once the
stimulus leaves.
iv. Physiologic hyperplasia:
1. Ex. Hormonal – breast and uterine enlargement during pregnancy
2. Ex. Compensatory – liver regeneration after partial liver removal
HYPERTROPHY:
 Compensatory – liver part cut off and regrows?
 Adaptive – CHF + bladder
v. Non-physiologic hyperplasia: due to excess hormonal stimulation or the
effects of growth factors on target tissues
c. Metaplasia = reversible! one cell type converts into another cell type
that can better endure the change/stress (occurs when body goes into new
“environment”, if the stimulus is no longer present, cells will come into their
original type)
i. this occurs in response to chronic irritation or inflammation
ii. allows for substitution of cells that are better able to survive under
circumstances that a weak cell could not (must be same cell type…ex.

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epithelial cell could be converted into another type of epithelial cell,


but NOT to a connective tissue cell)
iii. ex. Barrett’s esophagus (squamous epithelial cells change to columnar
cells)
d. Anaplasia = loss of cell differentiation (in cancerous tissue);
i. differentiated cells go backwards;
ii. “anaplasia” literally means “to form backward”

2. HIV - lab values, transmission, (CD4 count) … (* Look for key words! 2

answers where CD4 count is low but second part of the Q is tricky) 
(3Q)
a. Transmission: through blood, semen, vaginal fluids, breast milk
b. CD4+ count of 200 or less = AIDS!

3. Hypersensitivity Reaction Types: (anaphylactic response… what is

body producing as a result of this response? vasoconstriction/dilatation


going on? (what kind of effects are we going to have what type of
release are from an anaphylactic response?)

a. TYPE 1 – IgE-mediated disorders ~ “Allergic, Anaphylaxis, Atopy”


i. Rapid immediate reaction, could be local or systemic!
ii. Involves CD4+ helper T cells, which leads to release of inflammatory
mediators from sensitized mast cells
iii. PATHO: Occurs when an allergen (dust, pollen, animal dander)
interacts with IgE antibodies (bound to mast cells, basophils,
eosinophils)  triggers release of histamine from mast cells 
histamine signals the changes associated with allergies (inflammatory
processes)  allergic reaction happens almost instantly (symptoms
within minutes)
iv. Examples:
1. allergic rhinitis (seasonal allergies)  some individuals will
develop an atopic rash called “urticaria” (hives) or atopic
dermatitis (eczema)

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2. allergic asthma by environmental triggers; this type is also


mechanism behind more serious conditions like peanut or bee-
sting allergies that can lead to swelling of throat/lips/tongue,
SOB, stridor, and anaphylactic shock
3. drug reactions
4. food reactions
5. allergy to animals
6. ANAPHYLACTIC SHOCK = life threatening condition in which
there is systemic HISTAMINE release – mechanisms; causes a
massive global VASODILATION, hypotension, an increase in
vascular permeability and significant fluid movement into the
tissue; TX epinephrine (raises BP via vasoconstriction)
b. TYPE 2 – antibody-mediated disorders (cytotoxic hypersensitivity) ~
“AntiBody”
i. IgM and IgE antibodies against cell surface
ii. “tissue-specific” antigen
iii. Usually immediate responses
iv. PATHO: process by which IgG or IgM antibodies bind to a cell to
cause cell injury or death (antibody-mediated cytotoxicity). The
antibodies produced by the immune response bind to antigens on the
patients own cell surfaces (instead of pathogens).
v. Examples:
1. hemolytic disease of newborns (when Rh- mother has a
second Rh+ child and the maternal IgG targets fetal RBCs)
2. grave’s disease – specific to thyroid tissue
c. TYPE 3 – complement-mediated immune disorders ~ “Immune Complex”
i. PATHO: tissue damage created by immune complexes (aggregations
of antigen + antibodies). These antibody-antigen complexes circulate,
get stuck in vessels, and stimulate inflammation, end result being
inflammation-mediated tissue damage and necrotizing vasculitis.
ii. Examples: Systemic LUPUS erythematosus
d. TYPE 4 – T cell-mediated disorders ~ “Delayed”
i. Delayed hypersensitivity reaction
ii. PATHO: 2 subtypes:

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1. Direct T cell-mediated cytotoxicity = involves cytotoxic T


cells coming and killing target cells
a. ex. pancreatic islet cells in type 1 diabetes patient
b. hepatitis
2. Delayed-type hypersensitivity = helper T cells secrete
cytokines that activate macrophages (which eat the antigen) and
induce inflammation (which damages tissue)
a. allergic contact dermatitis
b. hypersensitivity pneumonitis (farmers? Constantly
exposed to particles, insecticides over and over…delayed
reaction so months/years later all these foreign materials
start to accumulate and have a negative reaction)
c. stem-cell transplant (might initially take the stem cells
w/o any issues but eventually graph vs. host disease 
body starts to develop antibodies

4. CAD  (patho), + patho for atherosclerosis - know process, what is

actually going on with it when occurring)


a. CORONARY ARTERY DISEASE (CAD) = heart disease caused by

impaired coronary blood flow.


i. most common cause = atherosclerosis! (plaque build up in

the arteries).
ii. CAD is commonly divided into 2 types of disorders:

1. Acute Coronary Syndrome = represents a spectrum

of acute ischemic heart diseases resulting from


disruption of an atherosclerotic plaque.
a. unstable angina  rest doesn’t help with the pain,

erosion of the plaque that leads to transient on/off


episodes of vasoconstriction events)
b. non-ST elevated MI (NSTEMI)  persons without

ST-segment (Q wave) elevation are those in whom

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thrombotic coronary occlusion is NOT COMPLETE


or intermittent
c. ST-elevated MI (STEMI)  those with ST-segment

(Q wave) elevation are usually found to have


COMPLETE coronary occlusion on angiography
and many ultimately have Q wave MI.
d. Troponin elevation is most specific biomarker for

diagnosing MI
e. acute MI (could result from non-STEMI or STEMI)

2. Chronic Ischemic Heart Disease = recurrent and

transient episodes of myocardial ischemia and stable


angina that result from narrowing of a coronary artery
lumen due to atherosclerosis and/or vasospasm
a. Stable angina  relieved by rest + nitroglycerin

b. Variant angina  coronary arteries “spasm”;

temporary closing of the artery; occurs @


rest/minimal activity often at night
c. Silent myocardial ischemia  w/o angina pain;

happens w/ ex. diabetics b/c they have sensory


issues
iii. Causes spectrum of disorders: myocardial ischemia, angina,

myocardial infarction, heart failure, conduction deficits, and


sudden death
iv. PATHO: Plaque build up narrows coronary arteries,

decreasing blood flow to your heart…eventually the


decreased blood flow can cause angina, SOB, or other CAD
signs & symptoms; a complete blockage can cause a heart
attack
v. RISK FACTORS: cigarettes, high BP, high LDL cholesterol, low

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HDL cholesterol, diabetes, advanced age


b. ATHEROSCLEROSIS – hardening of the arteries; formation of fatty lesions
in the lining of the large and medium-sized arteries (like aorta + its
branches, the coronary arteries, and the vessels that supply the brain) …
affects not only coronary arteries but other areas of the body as well.
i. slow and progressive process
ii. RISK FACTORS: major risk factor is hypercholesterolemia (high blood
cholesterol levels - specifically LDL). Hyperlipidemia also plays active
role in formation of atherosclerotic lesions. Risk factors that can be
changed with lifestyle modifications: high cholesterol, cigarette
smoking, obesity and visceral fat, hypertension, and diabetes mellitus
(type 2)
Others include: increasing age, family Hx, and male sex (non-
modifiable)
iii. PATHO: injury to the vessel wall triggers macrophages to release
substances that cause inflammation. The inflammation makes the
vessel more narrow, and eventually may occlude the vessel or
predispose to thrombus formation causing reduction of blood flow.
iv. Thrombosis is the most important complication of atherosclerosis

5. Stress response  (what does body do, what will be increased, what

will not be increase…physiological responses)


a. increase SNS + decrease PNS
b. heart rate and BP increase
c. sweating
d. respiration rate increase (lungs dilate)
e. GI activity decrease (loss of appetite)
f. Cortisol release from adrenal cortex (has # of fxns including glucose release
from the liver stores (glycogen) for energy)  increase in blood glucose!

6. METASTASIS - cancer, what’s the most common way things

would metastasize?
a. Metastasis = process of cancer cells moving from their original site to a

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different site in the body; Gains access to blood and lymph channels to
metastasize to other areas (local to distant sites)
b. Where they metastasize depends…but medicine shows that there
are certain types of cancers that have a tendency to metastasize
to specific areas
i. ex. prostate cancer  tends to metastasize to bone
ii. ex. breast cancer  tends to metastasize to the lungs and
brain
iii. ex. liver cancer  tends to metastasize lung

7. What is cancer pathophysiology?

a. CANCER = disorder of altered cell differentiation and growth,

resulting process is “neoplasia” = new growth


i. Cell proliferation is process of cell division; an adaptive mechanism for
replacing body cells as needed (normally, this is regulated! so the # of
new cells being made (by division) is the same as the # of cells dying…
replacement)
1. Cell proliferation is increased in cancer but the cells are not
doing their purpose b/c they undifferentiated (not specialized)
ii. Cell differentiation is the “cell specialization” process. As cells become
more specialized (or highly differentiated), the stimuli that induce
mitosis
1. Cell differentiation is not present in cancer, so there is a
lack in cell specificity
iii. Apoptosis = programmed cell death to eliminate unwanted cells
1. Cancer inhibits apoptosis

8. Malignant vs Benign tumors – 3Q

a. BENIGN NEOPLASM
i. Well-differentiated cells clustered together in a single mass
ii. Usually the cells resemble the tissue of origin (meant to be there)
but continuously grow and develop into tumors, complications can

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occur when there is a mass invading a space (think about what else in
that space can be affected as a result), so benign tumors must still be
removed!
iii. Some benign tumors are also known for their ability to cause
alterations in body function by abnormally producing hormones
iv. The rate of growth is progressive + SLOW
v. Grow by expansion with no invasion of surrounding tissue  NO
METASTASIS!
b. MALIGNANT NEOPLASM

i. Un-differentiated anaplasia; and they have the ability to

break loose, enter the circulatory or lymphatic system, and


form secondary malignant tumors at different sites
ii. No resemblance to tissue of origin

iii. Faster growth

iv. Grows by invasion infiltrates surrounding tissue

v. B/c of their rapid growth, tend to compress blood

vessels/outgrow their blood supply causing ischemia and


tissue necrosis

9. TNM classification (given something...was there metastasis? node

involvement? not? (1 Q)
a. TNM classification system for clinical staging of cancer
i. T = size and extent of the main tumor.
1. TX = main tumor cannot be measured
2. T0 = main tumor cannot be found
3. T1,2,3,4 = refers to size or extent of main tumor (higher number = larger
tumor)
ii. N = number of nearby lymph nodes that have cancer.
1. NX = cancer in nearby nodes cannot be measured
2. N0 = no cancer in nearby nodes
3. N1,2,3 = refers to number + location of nodes that contain cancer (higher
number = more cancerous nodes)

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iii. M = metastasis
1. MX = metastasis cannot be measured
2. M0 = cancer has not spread to other parts of body
3. M1 = cancer had spread

10. use of ANTIOXIDANTS (main purposes...what trying to prevent?


a. ANTIOXIDANTS = natural substances that stop/limit the damage

caused by free radicals. Your body uses them to stabilize free


radicals (unstable atoms), preventing them from causing
damage to other cells. Ex. fruits, vegetables that are high in
vitamin A, C, E, beta-carotene, grains, meat, fish, poultry
b. Our cells constantly exposed to oxygen. Could be bad – b/c oxygen also
causes oxidation = body chemicals are altered and become free radicals
which over time can cause a chain reaction in your body that damages
important body chemicals, DNA, and parts of your cells. Believed to
contribute to diseases like CANCER.

11. PRESSURE ULCERS - risk factors (different ways you can


develop) + stages
a. RISK FACTORS: HTN, high cholesterol, type 2 diabetes, obesity,

smoking, family HX of early heart disease, lack of exercise, aging,


sweating/urine or fecal incontinence (level of skin moisture),
impaired circulation, decreased sensory perception, immobility,
decreased protein (needed for tissue repair), decreased vitamin C
(collagen synthesis), vitamin A (stimulates epithelial cells and
immune responses…note: excess vitamin A can cause excessive
inflammatory response that could impair healing)
i. Major risk factor - hypercholesterolemia

b. STAGES:

i. STAGE 1

1. intact skin

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2. non-blanchable

3. erythema

a. (blue/purple hues in darker skin tone)

4. no dressing!

ii. STAGE 2

1. partial-thickness loss (epidermis or dermis…or both)

2. blistering or shallow crater

3. ulcer drains

iii. STAGE 3

1. Full-thickness loss (subcutaneous tissue)


a. damage or necrosis of subcutaneous tissue that
extends to but NOT through the underlying fascia
2. Deep crater (w/o undermining of adjacent tissue)
3. Necrosis + drainage continues
4. Infection develops
iv. STAGE 4
1. Full thickness
2. Necrosis + drainage continue
3. Subcutaneous - extends to muscle and bone
4. Deep pockets of infection develop

12. RISK FACTORS FOR THROMBI FORMATION :


a. prolonged bed rest

b. birth control pills

c. obesity

d. pregnancy

e. smoking

f. injury or surgery

g. cancer

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13. Leukemia - AML vs ALL (what type of lab findings?)


a. AML  ACUTE MYEOLICYTIC LEUKEMIA
i. Immature granulocytes that proliferate and accumulate in bone
marrow
ii. 50-55 year olds
iii. leads to anemia, neutropenia, and thrombocytopenia
iv. R&R  a standards DX criterion for AML is that more than 30% of
hematopoietic cells are myeloblasts
v. DX: bone marrow biopsy

vi. Google  Acute myeloid leukemia (AML) is a cancer of


blood-forming cells in the bone marrow. Abnormal immature
white blood cells (blasts) fill the bone marrow and spill into
the bloodstream.
b. ALL  ACUTE LYMPHOCYTIC LEUKEMIA
i. immature lymphocytes (increase in immature WBC) that proliferate
and infiltrate the bone marrow
ii. most common in CHILDREN (ages 2-10 years)
iii. R&R  CNS manifestations most common in lymphocytic leukemia
iv. DX: lumbar puncture
c. LAB FINDINGS for AML & ALL:
i. Presence of immature WBCs blast in the circulation and in the bone
marrow (60-100% of the cells)
ii. Definitive DX of acute leukemia based on blood + bone marrow
studies. Requires a demonstration of leukemic cells.
iii. R&R: Infection is a common presenting factor in acute leukemia, but
signs & symptoms may be absent because of neutropenia (a
decreased in neutrophils)

14. VERCHOW’S TRIAD - what are the risk factors for the
development of thrombi? SELECT ALL THAT APPLY (hyper
coagulability state…)

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a. 3 broad categories that are though to contribute to thrombosis (if


you have any of these 3 things, you are at risk for clot formation):
i. vessel injury
ii. venous stasis (slow moving of blood will cause pooling,
blood is not moving to the heart, incompetent veins)
iii. hypercoagulability – too much clotting present (increased
platelet function…conditions like atherosclerosis, diabetes
mellitus, smoking, increased blood lipid levels or blood
platelet levels)
1. people more likely to be in hypercoagulability state 
conditions associated with accelerated activity
a. malignant diseases – ex. cancer patients, deficient
in anticoagulant properties so might have a
deficient of proteins like antithrombin III, protein C,
+ plasmin)
b. pregnancy
c. use of oral contraceptives
d. post-surgical state
e. immobility
f. CHF

15. what age group affected by either AML or ALL (50 yr old, 4 or 3-yr
old) … should have idea of what type of cancer it is coming in

16. GERD (patho)  physiological relaxation of the sphincter!


a. disorder involving the reflux of stomach contents, causing unfavorable
symptoms or complications for the person such as regurgitation and
heartburn (pyrosis)
b. symptoms are short lived and occur after eating
c. the reflux is due to transient relaxations of weak or incompetent lower

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esophageal sphincter (basically the valve doesn’t close tightly enough or


it relaxes at the wrong time)
d. HEARTBURN 30-60 minutes after meals, evening onset, pain in epigastric
area that can radiate to the chest or arms
e. H. PYLORI = biggest risk factor for GERD + peptic ulcer disease
f. Various factors can lead to GERD:
i. Weakened esophageal sphincter
ii. Increased abdominal pressure (obesity or pregnancy)
iii. Hiatal hernia
iv. Medications (like morphine, Ca+ channel blockers, anticholinergic
agents, etc)
g. Avoid large meals
h. Avoid alcohol use and smoking
i. Eat meals sitting up
j. Avoid recumbent position several hours after a meal + bending long time
k. Sleep with HOB elevated
l. Lose weight if overweight

m. COMPLICATIONS = BARRETT’S ESOPHAGUS: In Barrett's


esophagus, normal tissue lining the esophagus changes
to tissue that resembles the lining of the intestine.
Increases the risk of developing cancer of the esophagus
(small risk though)

17. Gastroenteritis S&S:


a. pain, cramping, belching, nausea, vomiting (severe cases:

hematemesis), diarrhea

18. IBDs vs. gastroenteritis (be able to differentiate the two)


a. Gastroenteritis = inflammation of the stomach and intestines typically due
to bacterial or viral infection causing vomiting and diarrhea; ACUTE
b. IBD = inflammatory bowel disease  both produce inflammation of the

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bowel and autoimmune diseases; exacerbations + remissions; CHRONIC


i. Crohn’s disease – most commonly affects the distal small intestine
and proximal colon, but can affect any area of the GI tract from the
esophagus to the anus; cobblestone lesions (skipped lesions)
ii. Ulcerative Colitis – continuous + confined to the colon and rectum;
frank blood

19. PANCREATIC CANCER (mostly clinical presentations) (2Q)


a. Nausea/vomiting
b. Malaise
c. Diarrhea
d. Constipation
e. Palpable abdominal mass
f. Hematemesis – blood in vomit
g. Melena – blood in stool
h. Clay-colored stools (bile duct obstruction?)
i. Fatigue
j. New onset diabetes, not associated with weight gain
k. Jaundice
l. Upper abdominal pain
m. Weight loss
n. Pain with eating

20. Differences b/w Crohn’s vs UC

21. hepatic encephalopathy (know what it is)

22. Portal HTN:


a. low albumin b/c liver failure (or cirrhosis, malnutrition), so instead of the
blood flowing into the liver and then into the heart thru SVC/IVC, so instead
now the blood backs up into the vessels that are part of the hepatic portal
system... so now you have all this fluid accumulated in your vessels (the
ones in portal system), so your interstitial fluid hyperosmolar now. Fluid is

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going to move into the interstitial space


b. basically – if albumin is low (plasma protein), the blood in the portal system
is going to be hypo-osmotic, meaning that the water is going to want to
leave those vessels and move out into the interstitial space (creating edema,
ascites)
c. CAUSES: liver cirrhosis, liver failure, malnutrition, etc

23. NSAIDs how they affect peptic ulcer disease


a. NSAIDS impair the mechanisms that protect the gastric mucosa from the stomach acid
b. Aspirin and NSAID medications inhibit prostaglandin (inhibit mucosal prostaglandin
synthesis) which helps protect the lining of the stomach

24. ACUTE PANCREATITIS – what’s the first intervention? NPO b/c


their enzymes are eating away + if keep eating, the body will create
more enzymes and can auto-digest its own pancreas by eating itself.
a. when the pancreas is injured and/or function is disrupted, pancreatic
enzymes leak into the pancreatic tissue and initiates “auto-digestion”;
pancreatic enzymes destroy its own tissue, leading to inflammation. As a
nurse, you will make sure this patient is NPO STATUS in order to decrease
the enzyme secretion.

25. differences b/w hepatitis (ABCD) - 4 Qs

a. Hepatitis = acute/chronic inflammation of liver;most common


cause - viral
b. TYPES:
c. HEPATITIS A  fecal/oral; ACUTE form of the virus, body often able to clear
itself of the infection and no further complications occur. Spread through
eating or drinking water contaminated by feces of an infected person with
Hep A virus. Raw shellfish that has been water contaminated by sewage
may also spread the virus.
i. Incubation = 25-30 days
ii. RNA virus

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iii. Clinical: fever, malaise, jaundice, anorexia, N/V


iv. Hep A vaccine
v. No chronicity
vi. No carrier state
d. HEPATITIS B  blood/serum/prenatal ~ “B for Babies” – transmitted via
infected BLOOD or other BODILY fluids (saliva, semen, vaginal). Mother
may pass it to her child during childbirth.
i. Incubation = 60-90 days
ii. DNA virus
iii. Fever, fatigue, ABD pain, N/V, jaundice, joint pain, clay-colored stools
iv. Chronicity: Chronic hepatitis, hepatic necrosis
v. Hep B vaccine
e. HEPATITIS C  blood/serum  no vaccine! CHRONIC infection most often
develops; this form is spread through blood-to-blood contact through sharing
needles or needle sticks.
i. Incubation = 2-26 weeks
ii. RNA virus
iii. Fatigue, weight loss, anorexia, jaundice
iv. Chronicity – liver failure, liver cancer, cirrhosis
f. HEPATITIS D  blood/serum ; DEALIN’ WITH B  only found in people
who are already infected with hepatitis B b/c it is an incomplete virus
(requires a helper function from HBV to replicate). So if a person is infected
with Hep D they will also have Hep B.
i. Incubation = 30 days
ii. RNA virus
iii. Clinically – similar to Hep A
iv. Chronicity – yes
v. Hep B vaccine
g. HEPATITIS E  fecal/oral  no vaccine! EATING or DRINKING water that
has been contaminated by infected person’s feces, also raw shellfish
contaminated by sewage water. Very similar to Hep A but there is no
vaccine!
i. Incubation = 40 days
ii. RNA virus

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iii. Clinical – super infection


iv. Chronicity – high mortality rate
v. No carrier state

26. Who is most at risk for developing Pancreatitis?  ALCOHOLICS!


(also most at risk for hepatitis) … also non-compliant diabetics @ risk
as well.
a. Alcohol is metabolized by the pancreas and promotes the

synthesis of pancreatic digestive enzymes!

27. pneumonia - what is the most common or most causative


organisms

28. ARDS - classmate presentation (3Q)


a. ACUTE RESPIRATORY DISTRESS SYNDROME  severe form of acute lung
injury
i. characterized by sudden progressive pulmonary edema, increasing
bilateral infiltrates on chest X-ray, reduced lung compliance,
surfactant inactivation causing alveolar collapse (occurs without L
sided heart failure)
1. Infiltrate= alveolar spaces are filled with fluid
Intrapulmonary shunting of blood (so, the blood that goes back to
the heart is not oxygenated); permeability of the alveoli increases;
decrease in surfactant of alveoli; can lead to fibrosis,
ii. PATHO:
1. exudate enters alveoli
a. blocks gas exchange
b. makes inhalation more difficult
2. neutrophils enter alveoli
a. release inflammatory mediators
b. release proteolytic enzymes
iii. Manifestations:

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1. rapid onset of severe dyspnea (12-18 hours after initiating


event)
2. CXR  pulmonary edema and BILATERAL infiltrates (must be
bilateral to be considered ARDS)
3. Altered mental status (change in LOC)
4. Hypoxia
5. Tachycardia
6. Febrile
7. Acid-base imbalance
a. Respiratory acidosis = decreased pH due to decreased
ventilation and increased pCO2
b. Respiratory alkalosis = increased pH due to increased
ventilation and a decreased in pCO2

29. Respiratory - know LAB values! associated with COPD patients,


how to manage COPD pts, complications of COPD
a. with any type of respiratory issue, the first sign is always
RESTLESSNESS, confusion, altered mental status
b. RESPIRATORY LAB VALUES:
i. pCO2 = 35-45
1. pCO2 greater than 50 = hypercapnia (acute resp.
failure) w/ acidemia (pH < 7.3)
2. pCO2 greater than 45 = ventilatory failure
(ventilation is inadequate; problem is with oxygen
intake)
ii. pH = 7.35 – 7.45
1. acidemia = pH less than 7.3
iii. spO2 = 85-100%
1. spO2 less than 90 – acute resp. failure
iv. paO2 = 80 – 100 mmHg
1. paO2 less than 60 = hypoxemia (acute resp. failure) -

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cyanosis
v. HCO3 = 21 – 28
vi. O2 sat = 95 – 100%

c. ~ COPD ~ . IRREVERSIBLE; inflammation + fibrosis of


bronchial wall
i. EMPHYSEMA  airway collapse – weakened and
collapsed air sacs w/ excess mucus. Obstruction occurs
because of tissue changes rather than mucous production
which is the case in asthma and chronic bronchitis. LOST
ELASTICITY + HYPERINFLATION OF LUNG (overstretching
of lung tissues causes elastic components of lung to lose
their recoil, so its easier for the lung to inflate (inspiration)
BUT more difficult to deflate (exhale) because of the inability
to recoil). Elastic fibers are destroyed, so airways become
collapsible, small, obstructed.
1. Pink puffers, barrel chest, CO2 retention, chronic
respiratory acidosis, LOW paO2 level (hard for O2
to move from diseased lung to the bloodstream)
2. High levels of PROTEASES (emphysema is thought to
result from the breakdown of elastin + other alveolar
wall components by enzymes called proteases, which
digest proteins)
a. increased levels damage alveoli + small airways
by breaking down elastin  alveolar sacs lose
elasticity  small airways collapse or narrow 
some alveoli destroyed + others enlarged –
decreased surface area for gas exchange).
3. BULLAE = overstretching and enlargement of alveoli
ii. CHRONIC BRONCHITIS  airway inflammation +

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secretions
1. Chronic inflammation of bronchi + bronchioles caused
by chronic exposure to irritants (irritants trigger
inflammation  vasodilation, congestion, mucosal
edema, and bronchospasm)
2. Affects AIRWAYS ONLY - NOT ALVEOLI
3. Chronic inflammation  increase # and size of mucous
glands and increase mucous production!
4. Decrease pAO2 (hypoxemia) and increased pCO2
(respiratory acidosis)
5. “Blue bloaters”
iii. COMPLICATIONS OF COPD:
1. Affects oxygenation and tissue perfusion to all tissues in
body
2. Hypoxemia + acidosis
3. Respiratory infection (b/c mucous accumulation and not
coughing it out…ENCOURAGE FLUIDS +
COUGHING!)
4. Cardiac failure (cor pulmonale = increase strain on
the R side of heart due to lung disease, so you’ll have
an increase pressure of blood flow through the lungs)
5. Cardiac dysrhythmias
iv. CONSEQUENCES COPD:
1. Decreased ability to exhale (b/c mucous productions)
2. Stale air in lungs
3. Low O2 levels
4. High CO2 levels
v. Arterial blood gases show hypercapnia and hypoxemia
vi. FEV1: will decrease

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vii. Chest x-ray: show flattening of diaphragm because the lungs are filled with trapped air.
viii. Complete blood count: polycythemia, increase hemoglobin concentration
ix. When the patient goes into a respiratory failure the first thing the doctor checks is
Arterial blood gas (ABG) labs
x. Increased CO2 retention: hypercapnia. Because you can’t exhale the CO2.
xi. The most common indication seen in a patient is respiratory acidosis, pH less than 7.35.
xii. COPD can’t be cured but you can slow it down. STOP SMOKING!

30. ABGs too, WBC, CBC, Na serum levels, etc


a.CBC
i. Serum osmolality = 200 – 300 mOsm (book: 280-300)
ii. HbA1C = 4 – 5.5%
iii. WBC = 5,000 – 10,000
iv. Hemoglobin = 12 – 18 g/dL
v. Albumin = 3.5 – 5.5 g/dL
vi. Creatinine = 0.4 – 1.5 mg/dL
vii. Hematocrit = 40- 50 %
viii. Blood Urea Nitrogen BUN = 17 – 18 mg/dL
ix. Na serum = less than 200 mg/dL

31. ASTHMA  patho, risk factors, clinical manifestations (how will


patient look when assessing them?
a. PATHO – “REACTIVE AIRWAYS” … chronic disorder of the airways
that causes episodes of airway obstruction, bronchial hyper
responsiveness, airway inflammation, and allergies!
i. Elevated IgE; eosinophils… histamine release =
inflammation, vasodilation (which ultimately leads to
BRONCHOSPASMS/” bronchoconstriction” (contraction of

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smooth muscle in lungs); and thick mucosal secretions in


alveoli further impairs gas exchange
ii. Bronchial asthma = REVERSIBLE
iii. Asthma more r/t allergies, histamine release, mast cell
degranulation (leads to histamine release, cytokines, etc.)
iv. Triggered by cold air, high altitude, strong odors, emotional stress
(bronchospasm by vagal pathway), hormone changes, allergens, and
exercise.
v. Bronchial asthma affects AIRWAYS ONLY, not alveoli!
vi. With poorly controlled asthma, inflammation can lead to
hyperplasia of the bronchial epithelial cells + smooth muscle
b. RISK FACTORS – biggest  genetic predisposition for development
of IgE mediated response to common allergies. Other risk factors for
childhood asthma  family history of asthma, allergies, antenatal exposure to
tobacco smoke, and pollution
c. CLINICAL MANIFESTATIONS 
i. Complaints of air hunger and chest tightness
ii. SOB
iii. Anxiety
iv. use of accessory muscles
v. tachypnea (increase of respirations)
vi. tachycardia
vii. lung sounds such as WHEEZING
viii. long expiratory effort and diminished breath sounds in lower airways.
Coughing worse at night and morning. Wheezing during exhale.

32. MI- EKG changes


a. Acute myocardial infarction (AMI) = “STEMI” … ST-segment elevation

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MI
i. STEMI – most commonly transmural infarcts  involve the full
thickness of the ventricular wall (usually LV and interventricular
septum); most commonly with SINGLE ARTERY OBSTRUCTION
1. ST- segment elevation = Q wave elevation
2. Acute Myocardial Infarction – ischemic death of myocardial
tissue; remodeling and stunning (structural changes), the
myocardial cells lose contractility. Cardiac cells can withstand
ischemia for approximately 20 MINUTES after that irreversible
infarction
ii. NSTEMI – most commonly subendocardial infarcts  involve the inner
1/3 to inner ½ of the ventricular wall. Occur more frequently in
presence of severely narrowed but patent arteries
1. ST-segment depression = Q wave depression

33. understand atherosclerosis (not just plaque) - why is the plaque a


big issue? (5 q on atherosclerosis

34. CHF  what symptoms will patient have?


a. CHF = failure of the heart to pump enough blood to meet the metabolic
needs of the body
i. Decreased preload- volume in ventricle at the end of diastole; vol. after
filling!
ii. Decreased cardiac output
iii. Characterized by  Dyspnea and fatigue (mainly)
iv. RIGHT FAILURE  ~~~ “R” = “rest of body…fluid backs up to
rest of body”
1. Right ventricular dysfunction
2. PATHO: The RV cannot pump the blood out to the lungs, so it
is still receiving blood but cannot pump so the blood starts back
flowing into the systemic venous system!
3. may be secondary to respiratory problems (like COPD) – cor
pulmonale or a consequence of L sided heart failure.
4. R SIDED HEART FAILURE IS SYSTEMIC IN NATURE

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5. MANIFESTATIONS OF RIGHT <3 FAILURE:


a. Congestion of peripheral tissues  dependent edema
+ ascites
i. Liver congestion  signs R/T impaired liver fxn
1. Hepatomegaly (b/c of backflow)
ii. GI tract congestion  anorexia, GI, distress,
weight loss
iii. R sided heart failure is systemic in nature, if
the RV is not moving the blood forward, there
will be accumulation or congestion of blood
into the systemic venous system.
1. will see jugular vein distention,
peripheral edema, congestion,
hepatomegaly, may also see 3rd spacing 
accumulation of fluid in the interstitium
v. LEFT FAILURE  ~~~ “L” fluid backs up into the LUNGS
1. Left ventricular dysfunction
2. PATHO: impairs movement of blood from the (low pressure)
pulmonary circulation  (high pressure) arterial side of systemic
circulation
3. Normally, blood moves from high pressure (arteries) to low
pressure (veins); in left sided heart failure, blood accumulates
in the LV, LA, and the pulmonary circulation, which causes an
increase in pulmonary venous pressure.
4. Decreased CO
5. Decreased peripheral blood flow
6. Progressive accumulation of blood in pulmonary circulation
7. Decreased ejection fraction
8. Causes: HTN and AMI
9. MANIFESTATIONS OF LEFT <3 FAILURE:
a. Decreased CO  activity intolerance and signs of
decreased tissue perfusion
b. Pulmonary congestion
i. Impaired gas exchange  cyanosis + signs of

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hypoxia
ii. Pulmonary edema
1. Orthopnea
a. Cough with frothy sputum
b. Nocturnal dyspnea

35. PAD vs. PVD - assessment findings


a. Peripheral Artery Disease = arterial disease; causes S&S of of oxygen
deficit
i. Atherosclerosis is an important cause of PAD!
ii. Pain is intermittent claudication, relieved by dependent position (rest)
iii. Aggravating factors = activity (they have pain when walking),
elevation of legs
iv. Manifestations:
1. intermittent claudication = pain with walking
2. calf pain (b/c highest O2 consumption)
3. measure calf  ankle brachial index; anything less than 1 is
PAD;
4. vague aching,
5. numbness,
6. atrophic changes (cuz not walking)
7. SKIN = THIN, dry, shiny, cool, pale (skin pallor upon elevation)
8. cold temperature
9. weak pulses – diminished or absent
10. stasis ulcers – deep, pale ulcers located on toes, feet,
other areas of skin
11. gangrene = complication!
b. Peripheral Venous Disease - venous disease; S&S of metabolic waste
buildup
i. pain is aching/cramping aggravated by prolonged standing or
sitting
ii. pain is relieved by elevation of legs, lying, and walking
iii. Manifestations:
1. Peripheral edema

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2. Warmth/redness – red/brown pigmentation


3. Pulses present = normal or increased; bounding
4. SKIN = thick, tough, brown (brawny) pigment, normal
temperature, will have edema, varicosities
5. Venous stasis
6. Venous ulcers – superficial pink, over ankle
7. Poor healing = complication!
36. adrenal insufficiency + elevation…
37. ACTH (learn hormone what it does)
a. ACTH = adrenocorticotropic hormone produced by pituitary gland. Key
function is to stimulate production and release of cortisol from the adrenal
cortex.

38. Cushing’s Syndrome = hypercortisolism; ACTH is the


hormone responsible!
a. Three important forms of Cushing’s, results from from excess glucocorticoid production by the
body.
i. Pituitary forms = which results from excessive production of ACTH by a tumor of the
pituitary gland.
ii. Adrenal form =caused by a benign or malignant adrenal tumor
iii. Ectopic form = caused by non-pituitary ACTH-secreting tumor.
b. Can also occur by long term use of potent pharmacologic preparations of glucocorticoids
(Steroids)  LONG TERM STEROID USE!
c. Biggest clinical finding = HTN!
i. Stress, decreased healing, hyperlipidemia, buffalo hump, moon face, osteoporosis d/t
increased cortisol levels, hypokalemia as a result of hypernatremia, hirsutism, truncal
obesity, amenorrhea, etc.
39. DI – DIABETES INSIPIDUS: SELECT ALL; (pictures w/ diff signs
the person will exhibit)
a. LOW ADH (ADH is not secreted), so water is not retaining the

water
b. Pee a lot

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c. Increase Ht  blood will be more concentrated


d. Low BP + CO
e. High levels of serum osmolality

40. parathyroid lab values (don’t stress them but know NEG vs POS
feedback…)
a. low Ca+ in body  high PTH secretion

b. high Ca+ in body  low PTH secretion

41. PARATHYROID HORMONE (know talking about CALCIUM)


a. PTH  regulates Ca+ levels
b. increased PTH = increase calcium by stimulating osteoclast activity (to
break down the bone and release the Ca+)

42. Graves Disease


a. hyperthyroidism

b. decreased TSH

c. increased T3 + T4

43. diff bw type 1 + 2 diabetes

44. ADDISON’S DISEASE (2Q) – HIGH ACTH LEVELS! (compensatory, yet


no cortisol)
a. Adrenocortical insufficiency (hypocortisolism) = autoimmune destruction of
adrenal glands (most common cause)
b. Adrenal gland cannot produce glucocorticoids (cortisol), mineralocorticoids
(aldosterone), and sex steroids.
c. unable to conserve H2O and Na+ b/c they LACK ALDOSTERONE
d. Aldosterone deficiency
i. Low Na+ (d/t increased urinary loss of Na)  salt cravings!
ii. Low H2O (dehydration) (D/T loss of extracellular fluid
iii. Weak, fatigue
iv. CV collapse

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v. HYPOTENSION (LOW BP) as a result of hypovolemia


vi. Orthostasis (dizzy/light headed when stand because of insufficient
volume)
vii. Weight loss (vomit, diarrhea)
e. Cortisol deficiency
i. HYPOGLYCEMIA (rapid onset + progression of symptoms)
1. Think neurological symptoms! S/S are caused by:
a. altered cerebral function
i. headache
ii. difficulty problem solving
iii. disturbed/altered behavior
iv. coma
v. seizures
vi. mental confusion
b. activation of ANS (@ onset, PNS causes hunger initially,
but then SNS activation:
i. anxiety
ii. tachycardia
iii. sweating
iv. constriction of skin vessels (SKIN= COOL/CLAMMY)
ii. Lethargy
iii. Fever
iv. GI symptoms
f. ACTH elevation
i. Hyperpigmentation (bronze)  something about melanocytes
g. Tend to lack secondary sex characteristics (d/t lack of sex hormones) 
breasts, pubic hair, etc)
45. osteoporosis, osteomyelitis (3Q)
a. OSTEOMYELITIS acute/chronic infection of bone; usual cause is usually a
staph aureus infection in the bone, WBC will elevate (leukocytosis)…release
of lysosomes in this case pus starts forming in the bone (impaired blood flow
in bone), as a result can get sequestrium = necrotic/dead bone tissue.
i. TYPES:
1. hematogenous = infectious organisms reach the bone through

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bloodstream
2. contiguous spread = secondary to contiguous focus of infection;
direct inoculation from an exogenous source or from an adjacent
extraskeletal site
3. chronic osteomyelitis = occur secondary to an open wound
b. OSTEOPOROSIS  metabolic bone disease; porous bones; susceptible to
fractures; imbalance in bone formation vs. breakdown
i. Old bone is being reabsorbed aster than new bone is being
made

46. acute glomerular nephritis


47. GU – 15 Qs
a.ACUTE RENAL FAILURE
i. Abrupt onset
ii. Decreased GFR
iii. uremia
iv. Elevated BUN and creatinine (if the kidneys are failing, so they are
not removing the waste, therefore urea, nitrogen, and creatinine will be
present in high levels in the blood…creatinine is a metabolic end
product from the metabolism of creatine)
v. Hyperkalemia (normally, healthy kidneys will adjust the excretion of
potassium to match levels in consumption…but since they are failing,
not excreting K+)
vi. Metabolic acidosis (bicarb is not being excreted because kidney
failure)
vii. POOR PERFUSION! Is major issue?
viii. Most common

b. CHRONIC KIDNEY DISEASE


i. CHRONIC  Once patient has had Acute tubular necrosis –kidneys
try desperately to have some type of perfusion in attempt to prevent
actual kidney from dying…there is an increase in free radicals that
occurs in this process of trying to restore or maintain the kidney fxn,

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there will also be some acid base imbalances, kidneys also play big
role in absorbing / activating vitamin D (kidney disease you will have
issues with lower calcium levels, phosphate imbalance (vitamin D 
controls Ca+ and phosphorus levels in the blood), osteoporosis
sometimes b/c the kidneys absorb vitamin D and helps the body
absorb/maintain calcium and phosphorus levels
1. Causes:
a. Big one – HTN **
b. Anything that vasoconstrict … decreased flow
c. Smoking risk factor
d. Diabetes
e. Chronic pain medication use
f. Glomerulonephritis
2. Dx what stage do a biopsy
3. Renal insufficiency èup to 25%
4. Renal failure è is anything less than 20% of kidney fxn
5. Build up of waste, affects mind at risk for encephalopathy (a
disease in which the functioning of the brain is affected by some
agent or condition (such as viral infection or toxins in the blood).
6. Hyperphosphate, hypercalcemia, lactic acid elevated, risk for
CHF (b/c BP is off), risk for anemia (the RX itself is dialysis that
can cause hemolysis of the RBCs + platelet disfxn (so a lot of
peteichiae as well), confusion, encephalopathy
7. Decrease in EPO (erythryopoietin), as a result  anemia
8. Protein urea measures injury repair
9. Neuro complications – increased ammonia
10. Main clinical manifestation = UREMIA (accumulation
of nitrogenous wastes)
11. Skeletal disorders b/c of PTH (not enough Ca+ in the blood,
so there will be excess PTH which tells the body to pull the Ca+
out of the bone and into the blood)
12. Anemia + coagulation disorders  b/c EPO is decreased
13. “UREMIC FETOR” = urine-like odor in the breath
14. KNOW this pic:

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c.
d. UTI is a big cause of pyelonephritis

48. diff b/w pre-renal/post-renal failures, and intra-renal failures


(complications of glomerular nephritis)

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a.
b. PRERENAL FAILURE most common form of acute renal failure **
i. BEFORE KIDNEY  decrease in renal blood flow!
ii. Martinez: main thing to do with these patients is give tons of fluids to
perfuse the kidneys…mostly decrease in fluid or volume so
hypovolemic shock patients, clinically they will have less than 400 mL
of urine output a day (very little)….ultimately if you don’t perfuse the
kidney you will have ischemia  hypoxia  acute tubular necrosis
1. main cause of pre-renal failure = impaired perfusion (martinez)
2. Book: Causes of prerenal failure include profound depletion of vascular
volume (e.g., hemorrhage, loss of extracellular fluid volume), impaired
perfusion due to heart failure and cardiogenic shock, and decreased
vascular filling because of increased vascular capacity (e.g. anaphylaxis or
sepsis).
3. RESULTS:
4. GFR declines
5. Oliguria (~less than 400 mL of urine a day)
6. Ischemia  hypoxia  acute tubular necrosis (eventually)
7. Acute renal failure prerenal:

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a. Poor perfusion, hypovolemia, burns, decreased preload,


anything that decreased profusion to the kidney
b. PATHO prerenal failure: kidneys receive 20% of CO (very
little)
i. As renal blood flow falls  GFR down

c. INTRA-RENAL FAILURE
i. Martinez: associated with ischemia or any type of nephrotoxicity,
inflammatory, destruction of the actual renal tubules (actual kidney
itself), damage to parenchyma of actual kidney….
1. Ex. acute glomerulonephritis an acute inflammation of the
kidney caused by an immune response (formation of immune
complexes in the circulation that start to deposit into the
glomerulus, so you have activation of the IgG (any time u see IgG
usually it means that its gone? when you see IgM its an acute)
2. Caused by any type of injury as result of nephrotoxic medications
(can be caused by antibiotic TX, a malignancy, or HTN that is out
of control)
3. *TEST  pts that has strep throat can develop an acute post
strep glomerulonephritis (must treat patients quickly when
they have step throat) b/c the bacteria can transfer to the
kidneys; AMANDA  look up uric acid cast, myoglobulin, rhabdo
breakdown of muscle tissue?
4.
ii. Intrarenal renal failure or acute kidney injury, as it is now more commonly
known, results from conditions that cause damage to structures WITHIN the
kidney.
iii. The major causes of intrarenal failure are ischemia associated with prerenal
failure, toxic insult to the tubular structures of the nephron, and intratubular
obstruction. Acute glomerulonephritis and acute pyelonephritis also are intrarenal
causes of acute renal failure. Injury to the tubular structures of the nephron is
the most common cause and often is ischemic or toxic in origin.

d. POSTRENAL FAILURE

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i. Anything AFTER the kidneys (ex. ureters, BPH (benign prostatic


hypertrophy) Bladder
ii. Causes:
1. Bilateral ureteral obstruction
2. Bladder outlet obstruction
3. Prostatic hyperplasia: most common cause * (BPH)
iii. Pathophysiology
1. Results from obstruction of urine outflow (you have reflux of
urine back into the kidneys)
2. Ureters
3. Bladder
4. Urethra
5. Both of the ureters must be occluded to produce renal
failure

49. UTI = URINARY TRACT INFECTIONS


a. e. coli main bacteria causing the UTI
b. LOWER UTI = bladder  cystitis (inflammation of the urinary epithelium,
can be termed as:
i. complication  you have a UTI and don’t treat it w/ antibiotics and it
causes a “systemic” infection so it starts going up so you have renal
involvement, the systemic changes, fever, CVA tenderness, and patient
looks very sick.
ii. uncomplicated  “local” go to gyno and you have a UTI
c. UPPER UTI = kidneys  pyelonephritis
i. ACUTE PYELONEPHRITIS = severe upper UTI; abscess formation in
the nephrons and tubular necrosis; IVP determines kidney function
(look up); renal scarring and long-term damage. MAIN CONCERN =
tubular necrosis; hypoxia to the kidney occurs.
ii. S&S:
1. Flank pain
2. Pyuria (pus in the urine)
3. Look septic
4. Altered mental status

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iii. CHRONIC PYELONEPHRITIS


1. Can cause long-term hypertension
2. Decrease in GFR
3. Protein in the urine and glucose in the urine  because the
glomerulus is not working (not filtering)
4. Edema, HTN, and a decrease in the GFR when the glomerulus
itself is affected, the pores of the filter get bigger and bigger so
since the holes are not as small …and you have renal calculi
(kidney stones)
5. Atrophy and thinning of the renal cortex
6. 10-14 days for antibiotic TX to be considered effective
* Interstitial Cystitis = inflammation of the tissues in the bladder; when you hold your urine in
the bladder for hours, the pH of it changes, epithelium of the bladder changes and then you have
more risk of infection
* Normal bacterial flora:
- Lactobacillus in urethra of women
- Prostatic fluid protect urethra of men
* RISK FACTORS: hypospadias in men (urethra opening is on the underside of the penis),
impaired voiding (urine retention), ESTROGEN REDUCTION
* S&S: dysuria, acute cystitis (infection of bladder)  hematuria, a lot of times it’s a
foul smelling urine
* In a geriatric patient  classic sign of UTI present – change in mental status (LOC)
* URINE CULTURE  GOLD STANDARD for diagnosis of UTI = greater than or equal to
100k CFU/mL
(CFU = colony forming units)

50. GLAUCOMA (2Q)


a. chronic degenerative neuropathy

b. peripheral vision loss (visual field is loss)

c. increased intraocular pressure

d. open angle  LOW RATE of aqueous humor reabsorption!

i. the rate you produce the aqueous humor is higher than the

rate of reabsorption (you’re not reabsorbing that fluid), that


fluid accumulation compresses the optic nerve, pressure in

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your eye increases


e. closed angle  reabsorption rate is fine, but there is an

obstruction in the iris that is not letting the humor come out, so it
will stay inside and intraocular pressure will increase, compress
the optic nerve and the blood vessels
i. relief by sleep

51. Intracranial Pressure, TIAs, etc. (3Q)


a. epidural hematoma  develops b/w inner bones of skull + dura
i. tear in the MIDDLE MENINGEAL ARTERY
ii. ARTERIAL in origin
iii. Most common site = TEMPORAL region
b. subdural hematoma  develops in area b/w dura + arachnoid space
(subdural space)
i. VENOUS bleed
ii. Progresses SLOWER (b/c the subdural space is bigger than epidural
space, so youll see the blood slowly start to accumulate
c. traumatic intracerebral hematoma

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