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HD&T > Exam 2 study guide for final > Flashcards

Exam 2 study guide for final Flashcards

1
Q

Which of the folowing cells are least prone to injury

a. hematopoetic cells
b. Neurons
c. Hepatocytes
d. Testicular cells

A

B

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2
Q

Which cells are most prone to injury and why?

A

a. High metabolic cells and high proliferating cells are most prone to injuery because of their turnover and ability to get infected. High metabolic include :: liver, kidney, heart . High turnover is genital testicle, GI, hematopoetic cells.

• High metabolic cells

  • cardiac myocytes
  • renal tubular cells
  • hepatocytes

• Rapidly proliferating cells

  • testicular cells
  • intestinal lining cells
  • hematopoietic cells
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3
Q

Hypertrophy

A

a. Hypertrophy: increase in cell size

increased size of an organ or cell

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4
Q

Atrophy

A

decerased size of organ or cell or cell droopout

e. Atrophy: decrease in size of a muscle

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5
Q

Hyperplasia

A

b. Hyperplasia : increase in number of cells

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6
Q

metaplasia

A

replacement of once cell type with another

c. Metaplasia : one cell type changes to another

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7
Q

Dysplasia

A

disordered unregulated cell proliferation without maturation

d. Dysplasia: disorganized hyperplasia

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8
Q

Orderly cell death WITHOUT inflamm

A

apoptosis
-Apoptosis: non inflamm, programmed, req energy, happens in normal embryo, making fingers, normal cell turnoever, damaged cells, one cell ata time

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9
Q

Disorderly cell death WITH inflammation

A

necrosis

Necrosis – uncoordinated cell death, inflammation occurs, no need for ATP, cell membrane is disrupted, happens to cluster at a time., swelling due to loss of ion pumps

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10
Q

Death of a body part

A

gangrenous necrosis

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11
Q

Cell death occuring in granuloma

A

caseous necrosis

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12
Q

Irreverisble cell injury is more severe

A

Irreverisble cell injury is more severe: if you have a hole in cell membrane, long calcium influx, mitochondrial loss : types of irreversible cell injury are necrosis and apoptosis

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13
Q

A heart failure patient presents with hypertension he has some breathing problems that seem to be associated with pulmonary edema. He experiences dyspnea even when lying down. Papitation reveals a liver of normal size, which of the following is MOST LIKELY the cause of these symptoms

a. left sided heart failure
b. right sided heart failure
c. proportionate left and right sided heart failure
d. angina pectoris

A

-a
Left sided heart failure. This will cause back up into the lungs since the left side wont be able to pump out systemically leading to breathing problems and pulmonary edema.

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14
Q

left sided heart failure

A

Edema- lungs, congestion and edema too much extravascular fluid in tissues. Causes include hormone fluid retention, heart failure, inflamm
o Heart failure is common cause of pulmonary edema (especially left sided)

Left-sided failure:
-hypertension
-caused by ischemic heart disease
-pulmonary edema and breathing problems -orthopnea (dyspnea lying down)
-reduaced blood perfusion to organs, such as kidneys
causes prerenal zotemi high BUN, ATN

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15
Q

Right sided heart failure

A

Right-sided failure:
-Lung disease (e.g., Cor Pulmonale-abnormal enlargement of right side of the heart)
-hepatomegaly; pools in liver –chronic passive congestion
• Pathway to death, ischemic heart disease #1, hypertensive heart disease #2, valvular heart diseas #3

Ascites-massive peritoneal space fluid in liver failure because blood wont go through portal system !

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16
Q

c. proportionate left and right sided heart failure

A

both ascites in liver and trouble breathing

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17
Q

Angina pectoris

A

Angina Pectoris (know types, causes and consequences)
1. Stable angina
a. Pain, 2min, relates to exertion, relieved by rest or vasodilators, due to fixed
coronary stenosis
2. Variant angina
a. Occurs at rest, brief, reversible spasm
3. Unstable angina (most dangerous—prolonged pain or pain at rest)
a. Worsening angina, prolonged pain, due to acute plaque change like blew up

*chest pain to ischemia related metabolites accumulate (blood cant clean our garbage from cell fxn and metabolism)

Tx: with vasodilation drugs to increase flow
decrease o2 consuption (decreases metabolites) beta blockers, calcium channel blockers, decreases heart rate. and decreases work of how much heart has to do.

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18
Q

Select the incorrect statement of a myocardial infarction

a. as many as 10-20% of these patients experience NO pain
b. the majorirty of these patients experience pulmonary edema
c. these are often assoc with mural thromubs
d. typically precipitated by atrial premature beat.

A

d

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19
Q

Myocardial infarct

know symptoms and complications

A

C. Myocardial Infarct

  1. Symptoms, diagnostic criteria
    - restrosternal pain, dyspnea, diaphoresis, nausea, can be asymptomatic though
    - diagno 2 or more (ischemic chest pain >20 min, acute ekg change, rising falling of troponin, documentation of infarct)
F. MI complications:
• No symptoms (10-20%)
• Arrhythmias -95%
• Congestive heart failure 60%
• Pulmonary edema (60%)
• Pericarditis (50%)
• Mural thrombus (40%)
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20
Q

atrial premature beat

A

a. Increased rate of depolarization at any site to a rate faster than the sinus node is premature. (ectopic since comes from other area not sinus)

  1. Atrial premature depolarization-
  2. Ventricular premature depolarizations (VPBs)
  3. Junctional premature depolarization (av node/his bundle)
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21
Q

Select the incorrect statement

a. tachy arrhythmias are cardiac contraction rates of >100bpm
b. atrial fib is the most common inneffective cardiac contraction
c. essential hypertension is defined as elevated bp due to pheochromocytoma
d. hypertension caused by cognesitve heart failure wuld be considered secondary hypertension

A

c

essential hypertension has actually NO KNOWN CAUSE

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22
Q

Essential hypertension

A

Essential hypertension-(primary hypertension-it has NOT identifiable underlying
cause), and identify causes and consequences

a. Potential cause of essential hypertension is increased sodium retention and
intravasucular volume

b. Very common
c. Basically vessels are constricted in hypertension, kidneys see lack of blood flow and end up releasing renin, and inducing angiotensin. This increases sodium retention to make blood pressure go up. However as it keeps forcing up, it keeps damaging vessels causing damage.

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23
Q

Secondary hypertension

A

Secondary hypertension-(it is secondary to a separate underlying medical condition- e.x. CAUSED BY congestive heart failure) identify causes and consequences

a. Causes : endocrine, drugs, prego, renal failure, sleep apnea
b. Uncommon 5-10% of all hypertensive patients
c. Risk factors: black, old age, genetics, high salt diet, lack fo physical activity

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24
Q

Tachycardia

A

tachycardia > 100 bpm)

Causes of conduction disturbance: (what causes brady or tachy)

  1. Ischemic heart disease–scarring
  2. Degenerative changes
  3. Antiarrhythmic drugs
  4. hyperkalemia
  5. MI**
  6. Trauma
  7. Congenital
  8. Tachy-arrhythmias (rates usually > 100 bpm)—including re-entrant circuits -multiple ectopic foci (firing too frequently resulting in a circle/loop firing pattern)
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25
Q

atrial fibrillation

A 
Atrial fibrillation (MOST common-ineffective contractions)
-risk of thrombi in atria and embolizing (blood pools in atria)- accounts for 25% of strokes - flutter still contracts somewhat organized, fibrillation is chaotic (kinda reentry circuit) disorganized, and most common sustained arryhtmia in clinical cardiology.
  1. Often in congestive heart failure, valvular disease or hypertension
  2. 10% > 65 years of age have AF
  3. can lead to scarring
  4. inefficient cardiac output, high risk of thrombosis or embolization
  5. Can lead to ventricular fibrillation- know consequences
  6. Sudden cardiac arrest- know consequences
    - occurs when there is abrupt cessation of ventricle fxn due to rapid ventricular tachy OR ventricular fib. 90% fatal in cases.
    d. @ risk is patient swith coronary artery disease, heart failure, inherited channelopathis (electrical conduction problems)
    e. brain damage occurs in 4 min in SCA,
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26
Q

Which of the following is least likely to be a compensation for congestive heart failure

a. cardiohypertrophy
b. a reduction in cardiac stroke volme
c. increased catecholamine activity
d. tachycardia

A

C

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27
Q

Congestive Heart Failure

A

Congestive Heart Failure cardiac output is insufficient for metabolic needs of body

  1. Body’s compensation to heart failure (due to systolic, diastolc dysfuncton)
  • Tachycardia (increased heart rate)
  • Cardiohypertrophy
  • INCREASE in stroke volume (e.g., Frank-Starling mechanism
  • Increase catecholamine activity leading to positive ionotropic effect • Redistribution of blood flow (eg. Kidneys)
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28
Q

An elderly hypertensive man with type 2 diabetes has retrosternal chest pain every time he climbs stairs or otherwise exerts himself. The pain resolves 2-5minutes after he rests. it is ALSO* relieved when he takes nitroglycerine. The symptom pattern has been unchanged for the last 6 months. What is the LIKELY cause of the pain?

a. thrombus in coronary artery
b. fixed stable atherosclerotic stenosis of coronary artery
c. aortic dissection
d. pulmonary embolus
e. atrial fibrillation

A

B

Angina Pectoris (know types, causes and consequences)

  1. Stable angina
    a. Pain, 2min, relates to exertion, relieved by rest or vasodilators*, due to fixed coronary stenosis
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29
Q

fixed stable atherosclerotic stenosis of coronary artery

A

Angina Pectoris (know types, causes and consequences)

  1. Stable angina
    a. Pain, 2min, relates to exertion, relieved by rest or vasodilators, due to fixed coronary stenosis
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30
Q

thrombus in coronary artery

A

Coronary atherosclerosis

i. Cause 80% of heart disease
ii. Lesion can thrombosis, common sites are prox 2 cm of LAD LCX
2. Leading cause of death from heart disease (causes 80% of heart disease)
3. Link with stenosis (slow cause stable agina; abrupt causes thrombus/embolus)

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31
Q

aortic dissection

A

could be an MI

Myocardial infarct-symptoms
1. Can sometimes be asymptomatic
2. Scarring and its impact
3. What else could it be?
a. Pulmonary emboli, aortic dissection, pericardial tamponade
4. Dx criteria include @ least 2 : ischemic type pain over 20 min, acute EKG changes, rising then
fallig of cardiac biomarker like troponin, or patho document of infarct autopsy.

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32
Q

pulmonary emboli

A

could be an MI, or due to abrupt stenosis

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33
Q

Select the incorrect statement

a. valvular heart disease can be caused by strep infections
b. endocarditis can cause fatal thromboemboli
c. atrial premature beats are usually very dangerous
d. bradycardia is defined as fevewer than 60 bpm and can be caused by cardiac conduction blocks

A

c

*note: premature beats are not dangerous usually!

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34
Q

valvular heart disease

A

G. Valvular Heart Disease
1. define and relate to valvular heart disease—e.g., mitral valve
a. stenosis (aortic); valve won’t open
-aortic stenosis (post inflamm scaring in rheumatic heart disease, senile calcific aortic stenosis is most common,or calcified bicuspid valve.
-Calcific aortic valve stenosis (most common) (post inf endocardidits/rheum fever)
b. regurgitation (aortic)- can’t close completely
- post inflamm scarring, syphilitic aortisi, ankylosin spondyltisi
- mitral valve prolapse (large leaflets long chordae, wont close) , prone to
endocarditis
2. Types
• Rheumatic fever- systemic dsisae
• Infective endocarditis-dental procedure related. Types
-usually strep or staph (mitral valve 25% affects, tricuspid 10% affets)
• Often a pre-injured valve

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35
Q

Endocarditis can cause

A

Very destructive (mortality 70% if staph)
• Can cause thrombi (fatal as well!)
• Can destroy valvular tissue and cause perforations
• Infective endocarditis very dangerous
• Non cardiac – septic emboli

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36
Q

bradycardia

A

Definitions: bradycardia- 100 bpm)

a. Bradycardia – due to disturbance in impulse generation, impulse propagation, impulse propagation AV node to purkinje.
b. Lack of impulse propagation is conductinon block
i. Maybe you had a myocardial scarring, leads to fibrosis, cant generate
impulse through that hence conduction block

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37
Q

Select the incorrect statement concerning cardiac arrythmias

a. tachy-arrthmias can be caused by multiple ectopic foci
b. a risk of atrial fibrillation is a stroke causing emboli
c. often are associated with congestive heart failure
d. procainamide is first choice for ventricular arrythmias

A

d

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38
Q

Tachy-arrhythmias

A

(rates usually > 100 bpm)—including re-entrant circuits -multiple ectopic foci (firing too frequently resulting in a circle/loop firing pattern)

39
Q

Atrial fibrillation

A

(most common-ineffective contractions)

  • *-risk of thrombi in atria and embolizing (blood pools in atria)
  • accounts for 25% of strokes**
  • flutter still contracts somewhat organized, fibrillation is chaotic (kinda reentry circuit) disorganized, and most common sustained arryhtmia in clinical cardiology.
40
Q

whats is often associated in congestive heart failures?

A

Arrythmias / Ectopic beats

  1. Often in congestive heart failure, valvular disease or hypertension
41
Q

Procainamide

A

Na channel blockage (class 1 drugs)
Procainamide
• slows action potentioal conduction
• can precipitate new arrythmia
• effective for mostr atrial or ventricle arrythmia
****
• usually NOT first choice for cardiac arryhtmias

42
Q

Which of the following drugs is used to TREAT heart failre because of its ability to reduce heart rate and block sympathetic nervous system activity?

a. metoprolol
b. dobutamine
c. captopril
d. hydralazine
e. digitalis

A

Metoprolol

43
Q

Digitalis

A

B. Drugs
1. Positive ionotropic drugs
a. Mechanism: increases intracellular ca++ and cardiac contractility-in
turns increases blood ejection
b. Drug example: digitalis and Milrinone (bypridine)
c. Side effects
• Premature depolarization-arrhythmias (due to calcium overload exciting other parts)
• Ectopic beats
• Affects all excitable tissues

for heart failure**

44
Q

Hydralazine

A

Vasodilator

a. Drug: hydralazine
b. Mechanism: reduce pre- and post-load/ smooth muscle relaxant

for heart failure

45
Q

Captopril

A

ACE inhibitors (angiotensin-converting enzyme)

a. Drug: captopril
b. Mechanism: reduce peripheral resistance by reducing salt and water

Angiotensin affectors (block converting enzyme: block angiotensin I to II) inhibit
production of angiostensin
• ACE inhibitors and angiotensin II blockers-e.g., captopril

46
Q

Dobutamine

A

β1-adenoceptor agonists

a. Drug: usually dobutamine
b. Side effect: can cause arrhythmias

treats heart failure…activates contractions etc.

47
Q

Metoprolo

A

β-adrenoceptor blocker

a. Drug: metoprolol
b. Mechanism: reduce heart rate AND block sympathetic N.S.

for heart failure

48
Q

Select the incorrect statement concerning the following antihypertensive drugs

a. fureosemide is a loop diuretic more potent than hydrocholorthiazide
b. mannitol is an osmotic diuretic
c. Clonidine is an alpha 1 antagonist
d. Diltiazem is a calcium channel blocker
e. captopril is an ACE angiotensin converting enzyme inhibitor

A

c

49
Q

Fureosemid

A

Loop agents @ascending limb of henle (furosemide/bumetanide)-more
potent and more side effects

o Affects Na,k CL :
o Very efficacious
o More sodium, K, Cl in urine water follow (may end up causing
hypokalemia, NSAID sometimes stop loop diuretics)
§ Hypokalemia is problem since it can cause arrhythmia, also it leads to decrease in insulin secretion causing problems if
diabetic (causes hyperglycemia)
§ Loop diuretics increase cox2, NSAIDS block then and in turn
block loop diuretics

50
Q

Clonidine

A

Alpha 2 agonists - clonidine (common
o Central alpha 2 receptors in medulla is main mechanism
o If alpha 2 antagonist is given centrally, it blocks effect of clonidine.

 Agonist alpha 2: shuts down tone inmedulla 
- eatsallthebetas
- dereaseinbloodpressure
-drymouthandsedationarecommon
o
51
Q

Mannitol

A

Osmotic agent (mannitol) : not resorbed, water retained, near prox conv tubule

osmotic diuretic

52
Q

Diltiazem

A

calcium channel blocker

Calcium blockage (class 4 drugs)

  • Verampil and diltiazem
  • prolong refractory time
  • preipheral vasodilation
53
Q

captopril

A

ACE inhibitors (angiotensin-converting enzyme)

a. Drug: captopril
b. Mechanism: reduce peripheral resistance by reducing salt and water

54
Q

50 yr old patient tells you that her husband recetly had his cholesterol chcked and had a total of 290mg/dl and trigylceride of 200mg/dl . what drug is most likely used for both the high cholesterol and the triglyceride?

a. fenobrate
b. cholesteramine
c. exetimbe
d. lovastatin

A

D

55
Q

Fenobrate

A

Fibrates
(1) Mechanism:increases lipolysis in liver and muscles
(2) Actions:reducesVLDL,modesteffectonLDLandmoderate
increase in HDL, reduces triglycerides
(3) Drug:
• Fenobrate (Tricor)
(4) Toxicity:primarilyGIsymptoms

56
Q

Cholesteramine

A

Bile acid-binding agents

(1) Mechanism:reducesreabsorptionofbileacidsandmetabolite (which usually bind with fats and form cholesterol)
(2) Drugs:cholesteramine
(3) Sideeffects:constipationandbloating

57
Q

Exetimbe

A

inhibitors of intestinal sterol absorption

(1) ReducesLDL
(2) Drug:Exetimibe

58
Q

Lovastatin

A

Statins
(1) Mechanism:competitiveinhibitorsofHMG-CoAreductase
(synthesize cholesterol) (so stops cholesterol synthesis!)

(2) Drugs:
• Lovastatin (Mevacor)
• Atorvastatin (Lipitor)
• Simvastatin (Zocor)


(3) Actions:
• Reduce synthesis of cholesterol with most effect on LDL and some decrease in triglycerides—reduces coronary events
(4) Toxicity:
• Liver damage
• Weakness in skeletal muscles (increased CK)

59
Q

Select the incorrect statement concerning pulmonary pathology

a. asthma is associated with smooth muscle hypertrophy and hhper inflated lung
b. fibrosing lung disease are often associated with rheumatoid arthtiris
c. main cause of COPD is car emissions
d. Cystic fibrosis is associated with destruction of elastin and muscles in pulmonary bronchial walls

A

c

60
Q

asthma

A
  • Asthma is reactive, or happens due to something
  • Sudden (paroxysomal) You get narrowing of the airways a (bronchial hyperactivity)
  • Hyperinflated lungs/thick mucus plug (like chronic bronchitis but here there is muscle hypetrophy and eosinophil) /hyperplasia of bronchial glands/thickened basement membrane
61
Q

fibrosing lung diseases

A
  1. (restricting ) Fibrosing lung diseases (e.g., associated with collagen vascular diseases such as rheumatoid arthritis)-restrictive lung disease: stiff lung and hard to expand lungs
    a. deals with fibrosis, thick septal walls making gas exchange tough, less common than copd
    b. fibrosis makes lungs so hard to use that you have to breath harder to breath
62
Q

COPD

A

B. COPD (Congestive Obstructive Pulmonary Disease) (irreversible changes in airway)

  1. Causes:
    • Long smoking hx, or exposure to environmental irritants
    • Airflow limitations-due to progressive, irreversible airway remodeling
    • Obstruction in airway, airway has been remodeled, cant undo it !
    • Not fully reversible in contrast to asthma which can be at least partially reversible
63
Q

broncheostasis

A
  1. Bronchiectasis (obstruction of bronchi and persistent necrotizing infections): destruction of elastin and muscles in bronchial walls-congenital expression often caused by cystic fibrosis
    a. Happens because bronchi are obstructed (by mucus plug/tumors) and there are constant necrotizing infections (like TB or staph)
    b. The bronchial wall muscles, cartilage and elastin are all destroyed
    c. Congenital expression in ppl with cystic fibrosis
    d. Coughing up old stuff, blood, bad smell, if widespread you have hypoxemia with obstructive ventialtory defects
64
Q

which of the following drugs is described as a contrller agent and is most likely perscribed as primary drug for regular use to tx long term stable mod to severe asthma?

a. theophyline
b. montekulast
c. cromolyn
d. albuterol
e. fluticasone

A

e

65
Q

theophyline

A

c. Add-on controllers (tea, cocoa, coffee each contain a diff methxlanthine)
• Methylxanthine drugs; theophylline (tablet or inhaler)
(1) Mechanism: phosphodiesterase inhibitor and increases cAMP and relaxes airway smooth muscle by inhibiting MLCK (increase in camp will cause expansion)
(2) Monotherapy for mild asthma
(3) Combine with corticosteroids to reduce steroid doses and side effects (this will reduce severity of symptom in sever asthma)
(4) Monotherapy for mild acute asthama/ improves diaphragm fatigue in COPD/ need to monitor plasma levels/ stay less than 40mg/L to prevent toxicitiy issues like heart disease or seizures
(5) Toxicity: nausea, headache and anxiety

66
Q

montelukast

A

e. Leukotriene modifiers (inhibitors) (they are part of mast cell inflamm cascade, setting it off, triggering acute attacks) if this drug is takien regularly as prescribed you can inhibit attacks.
• E.g, montelukast (Singulair)
• Use is for prophylaxis-for patients who have trouble with inhaled therapies (e.g., nasal bleeding)-can take orally)
• This is important for patients who cannot inhale things without nose bleeds to take montekulast orally.
• Mechanism: block leukotriene-binding to receptor…leads to relaxed airway smooth muscle reduction of edema and diminished immunorxn activation

67
Q

Cromolyn

A

f. Cromolyn-inhibits release of inflammatory mediators such as histamine (mast cell stabilizer) (propylatic use only before exercise and allergen exposure)
a. If you nknow you are allergic to grass, and before cutting it that morning take this that means prophyltically.
b. -prophylactic use often before exercise—no rescue action (i.e., not a replacement for albuterol)

68
Q

Albuterol

A

a. Relievers (rapid bronchodilators B2agonists @ min dose and freq. Patients intolerant of B2agonst is req to inhale ipratropium bromide (not a resuce inhaler/takes 1 hr to get in) provide as a reliever) for ACUTE asthma
• Short-acting
• If you take them too long you will get tolerance..
• Less severe cases
• Typically beta2 agonist at minimum dose and frequency (intermittent)
o Beta 2 agonists will expand the airway helping in asthma
o Albuterol is fast, salmeterol is a slower onset.
o Mechanism : B2 agonsit increase CAMP, inhibits MLCK (myosin light chain kinase), gives bronchial relaxation
-e.g., albuterol ( Beta 2 agonist rapid onset and 4-6 hr effect); salmeterol (slower onset, 12 hr effectiveness)
• Mechanism of action: directly relax airway smooth muscle, side effect unusual if used properly
• Albuterol is the only rescue reliever (fast acting 15 min, effect 5hrs avg)
• Salmeterol (slower longer acting, 12 hr effect, expensive)

69
Q

controllers

A

b. Controllers (corticosteroids) ( taken regularly for long term control, inhaled agents like corticosteroids minimalize side effects alone or in combo)
• Take regularly for long-term stable control-often more side effects
• More for patients who aren’t being controlled with albuterol
• Inhaled: corticosteroids/drug of choice for moderate to severe asthma
-often combine with beta 2 agonists
-chronic management, not for rescue
-e.g., oral steroid is prednisone, inhaled is fluticasone – inhaled steroid, drug of choice for mod sever asthama who req B2 adrenergic drugs MORE than 1x day (-sone usually a steroid)
- common fluticasone+ salmeterol [advair diskus] for long term maintenance of asthma therapy. Fluticasone decreases bronchial reactivity by inhibit production of inflamm cytokines and infiltration of other cells.
-not a rescue drug used for chronic maintenance/not a bronchodilator
• Side effects: nose bleeds, sores in nose, mouth, tongue that don’t heal, thrush!
• Thrush, risk for slow growth in child, oropharnygeal candida tx w/ fluconazole

70
Q

Which of the following is responsible for majoiry of renal ureter stones?

a. magnesium ammonimu phosphate
b. calcaium oxalatae
c. uric acid
d. cystein

A

B

71
Q

magnesium ammonimum phosphate

A

b. Struvite (~10% of stones)-magnesium ammonium phosphate crystals-often associated with urinary infections-

ONLY type where treatment is to acidify urine.

a. Staghorn appearance like, do damage to smooth wall membrane of wall of ureter/kidney
b. Reasons why you acidify urine is because bacterial urease enzymes are alkalizing urine causing the staghorns!
c. More common in women!!!!

b. Trimethroprim – patients with struvities prevent or control urinary tract infection with abx

72
Q

calcium oxalate

A
  1. Types of kidney stones—usually alkalinize urine to treat, with one exception
    a. Calcium/oxylate excess in urine (~80% of stones)..so decrease oxylate rich foods!, or get parathyroid surgery.
    a. Raise pH of urine, alkalinze it which will shrink stoens to pass on their own! (take sodium bicarb tablets, etc)
73
Q

Uric acid

A

c. Uric acid-often associated with gout
a. More common in men
b. Deposits around joint of body
c. Urine mineralizes into stones when acidic

74
Q

Cysteine

A

d. Cysteine – must dissolve cysteine thus alkalize urine and increase water consumption to flush kidneys
a. Genetic condition dx in childhood

75
Q

Select the incorrect statement concerning pyelonephritis

a. most common cause is kidney stones
b. often associated with flank pain
c. 10-20% cause kidney failure
d. often causes kidney scarring

A

a…most common cause is infection

E. Pyelonephritis (10-20% kidney failure)
1. Define – urine is normally sterile, but with ascending infection you get inflammation in kidneys
2. Cause
• Retrograde (backwards ) spread from cystitis
• Common with urinary obstruction, stenosis
• Diabetes and immunocompromised (diabetes is the most common cause)
3. Consequences
• Flank pain
• Fever
• 10-20% chronic renal failure
• Kidney scarring
4. Can have acute or chronic (more scarring) types
a. Acute- pathchy neutrophils cast in urine, localized
b. Chronic- irregular scars under blunted calyces

76
Q

select the incorrect statement concerning urogenital diseases

a. majority of renal cancers are renal cell carcinomas
b. 3 weeks of complete urinary tract obstruction by a stone typically causes permanent kidney damage
c. females tend to have more bladder infections cytitis than males
d. most freq drug tx for bact cytitis or urethritis is erythromycin

A

d…common tx is below

B. Urinary Tract Infections (UTIs)-include cystitis and urethritis
1. Features
a. Often caused by E. coli, especially in females
b. Common treatment abx
• Trimethoprim-sulfamethoxazole (cell metabolism inhibitor)
o Sulfonamides block dihydropteroate, tmp blocks dihydrofolate , blocks protein synthesis
• Amoxicillin + clavulanic acid (resistant bacteria a problem) (to inhibit beta lactamase)
• Ciprofloxacin (expensive)

77
Q

cystitis

A 
H.	Bladder
1.	Bacterial cystitis (causes edema)
a.	Contributing factors
a.	Pyuria and dysuria seen
•	Stones
•	Catheters
•	Short female urethras
•	Obstructions
•	Ecoli
78
Q

majority of renal cancers are renal cell carcinomas

A

F. Renal cell carcinomas
1. Properties
• 80-90% of renal malignancies—most frequent
• More common in males >40 yrs, and smokers
• Analgesic abusers (NSAIDS)
• Obesity

79
Q

urinary obstruction

A

C. Urinary Obstruction
• 3 weeks of complete obstruction causes permanent damage
• Get dilated ureter and hydronephrosis
• If distal to bladder can get dilated bladder with a thickening of the bladder wall
1. Hydronephrosis-unable to concentrate the urine

80
Q

protamine

A

used to treat heparin overdose

  1. Intrinsic pathway
    • Contact factors through factor XIa to Xa-this is measured by PTT (partial thromboplastin time)…give protamine for reversal here…its charged + whereas heparin Is – charged.
81
Q

streptokinase

A

dissolves an established clot

82
Q

warfarin

A

antagonized by vit k

83
Q

clopidragel

A

platelet aggregate inhibitor

c. Clopidrogel – antiplatelet drug works on ADP to prevent degranulation helping anticoagulant

84
Q

enoxaparin

A

actions similar to heparin

85
Q

which of the followin is INCORRECT about struvite mangesium ammonium phspahte kidney stoens and their tx?

a. they are second most common type of kidney stone 10-15%
b. must alkalainze urine pH to dissolve
c. tmp-smx is often given to prevent or control underlying UTI in these patients
d. More common in males than females

A

b…you MUST ACIDIFY THE URINE!!

86
Q

tmp smx

A

b. Trimethroprim – patients with struvities prevent or control urinary tract infection with abx

87
Q

40 year old woman is complaining of feeling chronic nervous. feels hot and sweaty, heart beats rapidly, throid feels big when palpated, her free thyroxine t4 is 3 (normal is .8-1.7) dx is?

a. dequervain thyroiditis
b. graves disease
c. hasimotos
d. nodular goiter
e. toxic nodule

A

graves b

88
Q

Graves disease

A 
Hyperthyroidism
1. Clinical findings
✓ Nervousness
✓ Hotandsweating
✓ Weightloss
✓ Muscleweakness/tremor
✓ Palpitations/tachycardia
✓ “thyroidstorm​”(knowsymptoms)
o fever, CHF(congestive heart failure), and Coma.

o Lab: elevated T4 or T3. Low TSH.
o Causese: graves disease and toxic multinodular goiter

hyperthyroidism, and exopthalmos

89
Q

Hashimotos

A

a. Hashimoto’s disease ​(t-cell related autoimmune disease)
● Autoimmune; usually females
● May start as hyperthyroidism followed by permanent hypothyroidism(​inflammation leads to destruction)
● Thyroid enlarges- then atrophies over years
● Most often in females
● Labs: high TSH, low free T3 and T4.
o Main cause in US
● Painless
● Subacute granulomatous thyroiditis is not be confused with hashimotos. This type is painful, and self limited.

90
Q

most appropariate tx with someone with graves disease is

a. t3 supp
b. t4 supp
c. antisermum for tsh
d. beta blocker and radioactive iodine

A

d

radioactive iodine is always good for stuff like graves disease
and beta blockers will do well decreaesing the heart rate etc.

91
Q

Hours after a thyroidectomy a patient gets spasms. Then diffuse invol contraction of many muscles tetany. Lab tests reveal less than normal levels of calcium in blood..what happened?

a. inadvertant removal of parathryoids at the same time
b. reaction to seizure meds
c. severe thyroid hormone def
d. surgery related ischemic event

A

a..really nothing has anything to do with this question but a. They could have easily cut the parathryoids at the same time which would cause a decrease in calcium levels @ blood.

92
Q

28 year old man is noted to have moderate hypercalemia (14.5mg/dl … normal range 8.9-10.1) found in routine chem test. He complains of anoerxiea, constipation, kidney stone and weakness. What is the cause?

a. pulmonary metastatiic carcinoma
b. multiple myeloma
c. thyroid hyperplasia
d. parathyroid adenoma

A

d

93
Q

Hypercalcemia

A

Hypercalcemia
1. Due to hyperparathyroidism
a. Primary
● A very common endocrine disorder; usually an adenoma
● Symptoms: osteoporosis (fractures), constipation, nonspecific weakness, anorexia, stones, peptic ulcers,
depression, or even coma
● “bones, stones, groans, and moans”
● stones- nephrolithiasis. Groans-peptic ulcer, pancreatitits. Moans- depression, confusion coma,
● Arrhythmias
(1) Treatments usually surgical ​(parathyroid adenoma)
(2) Metastasis and carcinomas are rare

94
Q

patient has enlarge tongue and pronathic jaw. Speaks with low voice. avg height, large hands, has failing eyesight 30 years old what does he have

a. parathyorid adenoma
b. hypothalamus infarct
c. anterior pituitary adenoma
d. post pituatiry deficiency
e. cushings

A

c

by having the adenoma they have more growth hormone
this is acromegaly

he is 30 so its past growth plate time

HD&T (7 decks)

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