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Clinical Medicine LAB - Professor Sample > Endo #3 > Flashcards

Endo #3 Flashcards

1
Q

Aldosterone release is simulated by ?

A

Stimulated primarily by the RAAS (angiotensin II)

Stimulated secondarily by ACTH

Hyponatremia (aldosterone help you keep it )

Hyperkalemia ( aldosterone helps you get rid of it )

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2
Q

Hyperaldosteronism from nonadrenal conditions ?

A

Renal vascular stenosis

Hyponatremia (diuretic use)

Hypovolemia - will raise aldosterone level

**if kidney feel ischemic (RAS) they are going to release renin into the system to increase Bp flow to raise the intravascular volume **

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3
Q

Primary Hyperaldosteronism ?

A

usually a tumor ( CONN syndrome) of adrenal gland - adolsterone secreting tumor

kidney is going to want to shut off the aldosterone so it is going to lower the renin to shut down the aldosterone but its not going to stop cause there is a tumor ( high aldosterone and low renin)

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4
Q

Aldosterone used to dx ?

A

hyperaldosteronism

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5
Q

Aldosterone done in conjunction with ?

A

plasma renin assay

**high ALD, low renin - CONN

renal vascular stenosis - high renin and high aldosterone ( ALD in response toAldosterone assay
renin and ALD is from RAS) **

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6
Q

Aldosterone assay consists of ?

A

24 hour urine

plasma blood sample

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7
Q

Which aldosterone assay is more reliable ? Why ?

A

24 hour urine

more reliable cause blood sample fluctuate

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8
Q

Plasma blood sample fluctuates with ?

A

Diurnal variation

Body position (Upright position increases)

Diet (sodium will decrease)

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9
Q

Testing for Hyperaldosteronism own notes ?

A

has to do with giving Na

make them hypernatremia and we should see aldosterone release is suppress - supression test

stimulation - hyponatremia ,

both these tests we are actually checking renin levels to tell us if it is increasing or decreasing

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10
Q

Renin function ?

A

Enzyme that converts Angiotensinogen to Angiotensin I

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11
Q

Juxtaglomerular cells stimulated renin release ?

A

Decreased renal perfusion

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12
Q

Juxtaglomerular cells suppressed renin release ?

A

Increased renal perfusion

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13
Q

Macula densa cells in DCT stimulated renin release ?

A

Decreased Na

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14
Q

Macula densa cells in DCT suppressed renin release ?

A

Increased Na

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15
Q

Sympathetic nervous system in response to, stimulate renin release ?

A

Upright position - OS HTN

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16
Q

Sympathetic nervous system in response to, suppressed renin release ?

A

Supine position

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17
Q

Potassium levels in the serum, stimulated renin release ?

A

Increased potassium

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18
Q

Potassium levels in the serum, suppressed renin release ?

A

Decreased potassium

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19
Q

Plasma Renin Assay (PRA) screening test ?

A

Measures the rate of Angiotensin I generation

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20
Q

Primary hyperaldosteronism A/R ratio ?

A

A/R ratio >20

ALD super high and renin trying to shut off = CONN syndrome

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21
Q

Study Table 2-44 in Mosby’s!!

A

Primary hyperaldosteronism

Renin stimulation test

Captopril test - supression test of renin

not testing for the renin - actually testing for the enzyme converting it

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22
Q

Pheochromocytoma ?

A

Tumors of the adrenal gland that produce catecholamines ( epi / norepinephrine) - in the medulla

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23
Q

PHEochromocytoma phenmonic ?

A

Palpitations

HA

Episodic sweating (diaphoresis)

**H is also for HTN

get flushed and heart beats fast, palpitations, terrible HA and diaphoretic and it happens every once in a while **

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24
Q

Pheochromocytoma tests ?

A

Metanephrine (Plasma Free)

24 hour urine for VMA, HVA, and catecholamines

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25
Q

Metanephrine (Plasma Free) Pheochromocytoma test ?

A

Metanephrine ( metabolites of catecholemaines)

Normetanephrine

abnormal plasma free test and maybe imaging to see the tumor

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26
Q

24 hour urine for VMA, HVA, and catecholamines Pheochromocytoma test ?

A

VMA

HVA

Catecholamines

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27
Q

Used as a tumor marker for neuroendocrine tumors ?

A

Serum chromogranin A

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28
Q

Pheochromocytoma: Serum chromogranin A, own notes ?

A

they release hormone and ezymes and typically the PHE is a neuroendocrine tumors ( flushing etc)

this is a degradation product of the tumor - if it is positive it is highly likely they have a the tumor

highly sensitive and not as specific

29
Q

Lipids own notes ?

A

more bad cholesterol the worse it is for you cause the good HDL has a protective effect on the arteries cause it brings LDL to be degraded

fish oil ( omega 3 fatty acids, olive oil, any oil that is liquid at room temp is good

LDL have a low density to get into the lining of the arteries and the singing gets then then they get High BP and then it rupture wall of plaque and clot formation and it become mobilized and cause stroke

smoking lowers HDL, exercise raises HDL

30
Q

Lipid Panel involves ?

A 
Total Cholesterol
LDL
VLDL
HDL
Triglycerides
31
Q

NL aldosterone suppression test ?

A

suppress aldosterone release by decreasing renin

32
Q

abnormal aldosterone suppression test ?

A

Primary aldosteronism

lack of aldosterone suppression

33
Q

NL aldosterone stimulation test ?

A

renin level increased

34
Q

Abnormal aldosterone stimulation test ?

A

Primary aldosteronism

slight or no response in renin level

35
Q

aldosterone stimulation test uses ?

A

Na restricted from diet

36
Q

aldosterone suppression test uses ?

A

Isotonic saline infusion

37
Q

LDL cholesterol <100 ?

A

optimal

38
Q

LDL cholesterol 100-129 ?

A

near optimal / above optimal

39
Q

LDL cholesterol 130-159 ?

A

borderline high

40
Q

LDL cholesterol 160- 189 ?

A

high

41
Q

LDL cholesterol > equal 190 ?

A

very high

42
Q

Total cholesterol <200 ?

A

desirable

43
Q

Total cholesterol 200-239 ?

A

borderline high

44
Q

Total cholesterol > equal 240 ?

A

high

45
Q

HDL cholesterol <40 ?

A

low

46
Q

HDL cholesterol > equal 60 ?

A

high

47
Q

What is on the Framingham Heart Study ?

A

gender

HDL cholesterol

DM

age

total cholesterol

Tx for HTN

Race

systolic BP

smoke

**you get a percentage of cardiovascular risk of them having a HA in 10 years

90% - then 90% risk of event in 10 years

DM is cardiovascular disease equilvanent - we assume they have cardiovascular disease **

48
Q

Diabetes as a CHD risk equivalent: 10-year risk for CHD ?

A

20%

around 20 % already if DM for coronary heart disease

49
Q

Diabetes as a CHD risk equivalent: High mortality with established CHD - High mortality with _______ .

A

acute MI.

50
Q

Diabetes as a CHD risk equivalent: High mortality with established CHD - High mortality with _______ .

A

post acute MI

51
Q

With the new focus on cholesterol testing (ATP4) tx will no longer be adjusted or targeted for specific ?

A

lipid value

52
Q

ATP4: current evidence shows that reduction in ASCVD events is accomplished by using ?

A

maximum tolerated stain intensity on specific population

  • *“every one does better with a statin”
  • *
53
Q

TC/HDL ratio ?

A

Elevated TC and lower HDL raises the ratio which is undesirable and increases risk of HA

lower the ratio = lower risk

54
Q

TC/HDL ratio example ?

A

TC = 240 but when u look at break down of HDL of 45 = then this is okay it is good

55
Q

TC/HDL ratio ( men) ideal ?

A

<3.5

56
Q

TC/HDL ratio ( men) moderate ?

A

3.5-5

57
Q

TC/HDL ratio ( men) high ?

A

> 5.0

58
Q

TC/HDL ratio ( female) ideal ?

A

< 3

59
Q

TC/HDL ratio ( female) moderate ?

A

3.0-4.4

60
Q

TC/HDL ratio ( female) high ?

A

> 4.4

61
Q

Addisons pneumoic ?

A

need to ADD hormone

62
Q

Cushing syndrome ?

A

have extra cushion of hormone

63
Q

Clinical ASCVD / age <75 w/o safety concerns, statin tx ?

A

HIGH

64
Q

Clinical ASCVD / age >75 w/ safety concerns, statin tx ?

A

moderate

65
Q

LDL > 190 w/o clinical ASCVD and >21 y.o., statin tx ?

A

High

66
Q

DM w/o ASCVD ages 40-75 with LDL 70-189, 10 yr risk ASCVD < 7.5, statin Tx. ?

A

Moderate

67
Q

DM w/o ASCVD ages 40-75 with LDL 70-189, 10 yr risk ASCVD >7.5, statin Tx. ?

A

High

68
Q

Non DM w/o clinical ASCVD, ages 40-77 with LDL 70-189, 10 years ASCVD risk >7.5, statin Tx. ?

A

moderate to high

Clinical Medicine LAB - Professor Sample (36 decks)

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