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Apex Pt 2 > Kidney, Liver, Endo > Flashcards

Kidney, Liver, Endo Flashcards

1
Q

What is in renal cortex

A

Glomerulus, Bowman’s capsule, proximal tubules, distal tubules

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2
Q

What is in renal medulla

A

Loops of henle and collecting ducts

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3
Q

What Aldosterone v adh does

A

Aldosterone- na and water absorbed (extracellular vol). ADH absorbs water (osmolarity).

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4
Q

Hormones made by the kidney

A

Renin, EPO, d3

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5
Q

Kidneys receive what % of CO. Of that what is filtered by glomerulus, what happens to other part

A

20-25. 20. Circulates through peritubular capillaries

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6
Q

Renal blood flow calc

A

(Map - renal venous pressure) / renal vascular resistance

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7
Q

Renal cortex v medulla blood flow and p50. Which area more sensitive to ischemia

A

Cortex= 90%, 50. Medulla= 10%, 10. Medulla more sensitive

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8
Q

RBF in neonate, when it achieves adult level

A

Doubles first 2 weeks of life. Adult level at 2 years old

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9
Q

How kidney autoregulates to maintain renal perfusion

A

When perf too low, bf inc by reducing vascular resistance. Vice versa is true

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10
Q

Renal blood flow autoreg range

A

Map 50-180

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11
Q

Most important methods of autoreg in kidney

A

Myogenic mechanism and tuboglomerular feedback

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12
Q

What increases renin release

A

Reduced renal perf, b1 activation, dec na and cl delivery to distal tubule

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13
Q

What things increase aldosterone release

A

High k, low na, RAAS stim

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14
Q

What controls adh release

A

Inc osmolarity of ECF and decreased blood vol

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15
Q

How adh restores bp

A

Stim v2 in CD, inc cAMP, aquaporin channels inserted into cd and stim water reabsorption. Stim v1 which vasoconstricts in periph vessels (IP3), inc SVR

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16
Q

Which anesthesia related things impact adh homeostasis

A

Inc by peep, pos pressure vent, hypotension, bleeding

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17
Q

How ANP acts

A

Produced in myocardium in resp to atrial distension. Stim na and h20 excretion in collecting ducts. Neg feedback to RAAS, inhib renin release

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18
Q

DA1 v DA2

A

1= in renal vasc and tubules, r/t inc cAMP, vasodilation/inc RBF+GFR/diuresis/na exc. 2= pre sns, dec cAMP, dec NE release

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19
Q

Calc: net filtration pressure in kidney

A

Glom hydrostatic p - Bowman’s capsule hydrostatic p - glomerular oncotic p

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20
Q

What conditions inc gfr and filtration fraction

A

Constriction of efferent arteriole and dec plasma protein

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21
Q

Most important determinant of gfr

A

Glomerular hydrostatic pressure

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22
Q

What determines glomerular hydrostatic pressure

A

Arterial bp, afferrent arteriolar res, efferent arteriolar res

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23
Q

Reabsorption

A

From tubule to peritubular capillaries

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24
Q

Secretion

A

From peritubular capillaries to tubule

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25
Q

Excretion

A

Removal from body in urine

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26
Q

Urinary excretion rate=

A

Filtration - reabsorption + secretion

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27
Q

Where is most of filtered na reabsorbed

A

Proximal tubule

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28
Q

Func of proximal tubule, what happens here

A

Bulk reabsorption of solutes and h20. 65% of h20, na, k, cl, and bicarb

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29
Q

Func of desc loop of henle

A

Water reabsorption, countercurrent inc osmolarity of peritubular fluid to achieve this

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30
Q

Ascending loop of henle function

A

K, na, and cl pumped into interstitium. Impermeable to h20. UF hypotonic. H excreted. Still countercurrent

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31
Q

Distal tubule func

A

Fine tunes solute conc. Na, k, cl, hco3 reabsorbed. Where aldosterone and adh act, only ways h20 is let in. Parathyroid hormone inc ca. Where juxtaglomerular apparatus is, adjusts urea conc

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32
Q

Collecting duct func

A

Regulates conc of urine. ADH inc h20 reabs, anp inhib h20/na reabs. Aldosterone works here. Adjusts h conc

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33
Q

How CAI diuretics work

A

Inhib carbonic anyhydrase, reduces reabsorption of hco3, na, and water in proximal tubule

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34
Q

Uses of CAIs

A

Open angle glaucoma, high altitude sickness, central sleep apnea

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35
Q

Complic of CAIs

A

Metabolic acidosis, hypokalemia, in COPD loss of hco3 may exac cns dep from hypercarbia

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36
Q

How osmotic diuretics work

A

Inhib h20 reabsorption in proximal tubule and loop of henle. They pull ECF into IV space. Good for brain bad for heart

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37
Q

Uses of osmotic diuretics

A

Prevent AKI, ic htn, dx acute oliguria (inc UOP if prerenal)

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38
Q

Complic of osmotic diuretics

A

CHF, pulm edema, if bbb disrupted will enter brain and cause cerebral edema

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39
Q

How loop diuretics work

A

Poisons na k 2cl transporter, lose dilute urine, k, ca, mg, and cl

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40
Q

Complic of loop diuretics

A

Hypochloremic metab alkalosis, pot nmbs, weakness, ototoxic, reduced lithium clearance

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41
Q

How thiazide diuretics work

A

Inhib na cl transporter in distal tubule. Inc serum ca and can inc bg

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42
Q

Complic of thiazide diuretics

A

High bg/ca/uric acid, low k, metab alkalosis, HLD

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43
Q

K sparing diuretics moa

A

Amigo ride and triad inhib k sec and na reabs in CD. Spironolactone = aldosterone antag, inhib k sec and na reabs in CD

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44
Q

Complic of k sparing diuretics

A

High k (inc if using nsaids/bb/ace inhib), metab acid, gynecomastia, libido changes, nephrolithiasis

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45
Q

Best tests of tubular func

A

Frac exc of na and urine osmolality

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46
Q

Tests of GFR

A

BUN and creatinine clearance

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47
Q

Bun <8 means what

A

Overhydration, dec urea produc (malnutrition or liver dis)

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48
Q

Bun 20-40 means what

A

Dehyd, inc protein input (diet, GIB, hematoma breakdown), catabolism (sepsis or trauma), dec gfr

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49
Q

100% inc in creatinine means what

A

50% reduction in gfr

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50
Q

Nml bun to creat ratio. If >20:1= what

A

10:1. If >= azotemia.

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51
Q

GFR calc

A

((140-age) x (kg)/(72 x creat)

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52
Q

Fe(na) <1% means what

A

More na conserved than creat cleared. = prerenal azotemia

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53
Q

If Fe na >3% means what

A

More na excreted than creat cleared. Means tubular func impaired

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54
Q

Prerenal oliguria looks like what w tests

A

Fe na <1, urinary na <20, osmolality of urine >500, ratio >20:1, nml sediment or maybe hyaline casts

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55
Q

Acute tubular necrosis looks like what in tests

A

Fe na >3, urinary na >20, urine osmolality <400, bun cr ratio normal. Tubular epithelial casts or granular casts

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56
Q

Uremic bleeding: cause, what is normal, tx

A

Dysfunctional platelets. Normal pt, ptt, and plt count. Tx is desmopressin, dialysis preop

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57
Q

Prop in renal pts dose and why

A

Inc dose, hyperdynamic circ and bbb disrup d/t uremia

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58
Q

Precedex use in renal pts

A

Liver metab, safe to use. Doa may be prolonged

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59
Q

Preventative strategies for contrast media induced AKI

A

Nacl, low/isoosmolar contrast, sodium bicarb

60
Q

SE and use of calcineurin inhib in renal pts

A

Immunosuppression for transplants. SE: htn, renal vasoconstriction

61
Q

Turp: level required for spinal. Resec time limit and solution height above table

A

T10. 1 hr or less. <30 cm above table

62
Q

Turp solution pro and SE: distilled water

A

Good for surgeon. Inc risk turp syndrome, dec, na, hemolysis, hemoglobinuria

63
Q

Turp solution pro and SE: glycine

A

Dec risk turp syndrome. Inc ammonia, dec loc, postop blindness

64
Q

Turp solution pro and SE: sorbitol

A

Dec risk turp syndrome. Hyperglycemia, lactic acidosis

65
Q

Turp solution pro and SE: mannitol

A

Osmolarity similar to plasma, no renal metab. Transient plasma expansion —> risk if lv fail

66
Q

Turp solution pro and SE: NACL

A

Absent of many se. Can only be used if bipolar cautery, cant use unipolar (current)

67
Q

Turp syndrome: triad, na level <120, na level <110

A

Hypertension (inc PP), bradycardia (reflex), alt LOC. <120= inc risk complic. <110 sz, coma, lethal ventric dysrhythmias

68
Q

Absolute contraindications to ESWL

A

Pregnancy, bleeding disorders, anticoagulation

69
Q

What removes bacteria from liver

A

Kuppfer cells

70
Q

Liver version: arterioles, capillaries, venule s

A

Term branches of hepatic a and portal v. Sinusoids. Central vein

71
Q

In liver, which zone best oxygenated, which worst oxygenated, which has highest conc of cp450 enzymes

A

Best= zone 1 (periphery). Worst= zone 3 (near central vein)). Highest cp450, zone 3

72
Q

Liver: % of CO, blood flow to liver

A
  1. Aorta to sphlanchnic to portal v to liver. Or aorta to hep artery to liver
73
Q

Portal vein: ___% of liver bf, ____% of o2 content

A

75% bf, 50% constant (lower o2 sat)

74
Q

Hep artery: __% bf to liver, ___% 02 content

A

25, 50 (higher constant)

75
Q

Portal htn dx: portal vein p, sinusoidal p

A

> 20, >5

76
Q

Hepatic artery perf p calc

A

MAP - hepatic vein pressure

77
Q

Hepatic arterial buffer response. What happens, what mediates it, what impairs it

A

Reduc in portal v flow compens by inc hepatic artery flow. Mediated by adenosine, impaired by severe liver disease

78
Q

Effect of anesthesia on hepatic BF

A

Dec MAP, can reduce hepatic bf 30-50%

79
Q

Procoagulants made by liver

A

Thrombopoietin, alpha 1 glycoprotein, factor 7

80
Q

Factor VIII is made in the _____ but not made by the _____

A

Made in liver. Not made by hepatocytes

81
Q

Albumin= reservoir for ____ drugs

A1 glycoprotein= reservoir for ____ drugs

A

Acidic. Basic

82
Q

AST/ALT ratio > ___ suggests cirrhosis or etoh liver disease

A

2

83
Q

most sensitive indicator of biliary duct obstruction

A

5 nucleotidase

84
Q

Bilirubin levels if damage: before liver, in liver, after live (cholestatic)

A

Before= inc unconjugated. In or after= inc conjugated

85
Q

Markers of hepatitis a

A

IgM early, IgG late

86
Q

IA that makes most trifluoroacetic acid, IA doesnt make any

A

Halothane. Sevo makes none

87
Q

RF for IA induced TFA/hepatitis

A

> 40 years old, female, >2 exposures, genetics, obesity, CYP2EI induction (etoh, isoniazid, phenobarb)

88
Q

Hepatitis: most common cause, 2nd most common. Dx of it

A

Etoh. Hep c. Inc liver enzymes, bilirubin, cell changes

89
Q

S/sx and lab changes w hepatitis

A

Jaundice, fatigue, low plt, glomerulonephritis, neuropathy, arthritis, myocarditis. Pt prolonged, dec albumin

90
Q

Anes consid to maintain hepatic bf

A

Use iso (preserves it), avoid peep (inc resistance to drainage), normocapnia, liberal IVF, regional ok if no coag alt

91
Q

Hepatotoxic drugs that inhib cyp 450

A

Tye, amio, halothane, abx (pcn, tetracycline, sulfonamides)

92
Q

Etoh withdrawal syndrome: when s/s appear, peak. Early and late s/s

A

Appear 6-8 hr. Peak 24-36 hr. Early: tremor, halluc, nightmares. Late: inc sns (hi hr and bp, dysrhythmias), Nv, insomnia, agit

93
Q

Tx etoh withdrawal

A

Etoh, BB, A2 agonists

94
Q

When DTs occur. S/s. Tx

A

2-4 days after no etoh. Grand mal sz, hi hr, hi or low bp, combative. Valium or benzos, BBs

95
Q

Tx drug for alcoholics in recovery. SE of it

A

Disulfiram. Hepatotoxic. Inhib dopa beta hydrozylase —> hypotension

96
Q

MELD: what it assesses. Low risk, high risk

A

Bilirubin, INR, and serum creatinine. <10. >15

97
Q

Child Pugh score: what it assesses, classes

A

Albumin, PT, bilirubin, ascites, encephalopathy. A= 10% risk periop morbid. B= 30. C= 80

98
Q

Child Pugh score: how class scoring impacts proceeding to surgery

A

A or B ok to surgery if optimized. C should be medically managed until function improves (hepatic)

99
Q

Drugs that relax sphincter of oddi

A

Glucagon, glyco, atropine, narcan, ntg

100
Q

Ant pituitary hormones

A

Fsh, lh, acth, tsh, prolactin, growth hormone

101
Q

T3 compared to T4

A

T3 has higher potency and shorter half life

102
Q

T3 is a ____hormone, T4 is a ____hormone

A

T3= prohormone. T4= active hormone

103
Q

Hypothyroid: lab alt, what causes goiter

A

Tsh chronically high. Thyroglobulin colloid causes gland to inc since tsh high

104
Q

How thyroid hormones effects heart

A

Inc contractility/rate/rate of relaxation, dec SVR

105
Q

How thyroid hormone effects resp and mac

A

Inc co2 produc __> inc vt and rr. No effect on mac. Dec rate of induc

106
Q

Effect of k iodide on hyperthyroidism

A

Reduces thyroid hormone synthesis and release, given 10d preop

107
Q

Drugs that inhib conversion of t4 to T3

A

Propranolol, esmolol, ptu, methimazole, carbimazole

108
Q

If emergent thyroid sx give what rx

A

Bb, k iodide, glucocorticoid, ptu

109
Q

Avoid what in thyroid surgery

A

Sympathomimetics, anticholinergics, ketamine, panc

110
Q

What thyroid storm can mimic under GA

A

MH, pheo, neuroleptic malignant syndrome, light anesthesia

111
Q

What Block’s thyroid synthesis

A

Methimazole, ptu, k iodide

112
Q

What Block’s thyroid release

A

Iodine/iodide

113
Q

Why aspirin bad in thyroid pt

A

Dislodges t4 from plasma proteins and inc free frac of t4

114
Q

Signs of hypocalcemia

A

Spasms, tetany, laryngospasm, mental status alt, low bp, prolonged qt, parasthesias, chvosteks and trousseaus

115
Q

Hypothyroid: rx given and initial response

A

T4, natiuresis and dec tsh

116
Q

Induction (inhalation) is ____ w hypothyroid

A

Faster

117
Q

Hormones made in: zona glomerulosa, fasciculata, reticularis

A

Mineralcorticoids, glucocorticoids, androgens

118
Q

How to remember what adrenal cortex zones release

A

Salt, sugar, sex

119
Q

Aldosterone causes what shifts

A

Na and h20 reabsorption. K and h excretion

120
Q

Aldosterone release is inc by what 3 things

A

RAAS activ, high k, low na

121
Q

Aldosterone regulates what, does not regulate what. Causes metabolic ___

A

Reg iv vol not osmolarity or na conc. Alkalosis

122
Q

What doesnt have glucocorticoid effects

A

Aldosterone

123
Q

What doesnt have mineralcorticoid effects

A

Decadron, betamethasone, triamcinolone

124
Q

Conns disease: excess ____. Features, anes implic, tx

A

Aldosterone. Htn, low k, metab alk. Give k, restrict na, give spironolactone. Sensitive to NDMR, u wave on ekg, avoid hypervent and vol overload (hypertensive)

125
Q

Cushings: k shift, metabolic ___, anes implic

A

Low k, alkalosis. Post op give steroid. May have DI after resection

126
Q

Signs of adrenal insuff

A

Low k, hi na, metab acid, low bg and bp, nv

127
Q

When pt should get stress dose of steroids preop

A

> 20 mg/day prednisone (80 hydrocortisone) for over 3 weeks

128
Q

Hydrocortisone if minor, moderate, or major sx

A

Minor: 25 mg. Moderate: 50-75 mg. Major: 100-150

129
Q

Hormone released by pancreatic cells: alpha, beta, delta

A

Glucagon, insulin, somatostatin

130
Q

Drugs that inc or dec blood glucose

A

Inc by beta agonists. Dec by BB or VAs

131
Q

What stim v inhib glucagon release

A

Stim: decreased glucose, stress, sepsis, trauma, b agonist. Inhib: inc glucose, insulin, somatostatin

132
Q

What somatostatin does

A

Inhibits insulin and glucagon. Dec sphlanchnic bf and dec motility

133
Q

Biguanides (metformin): key facts/risks

A

Doesn’t cause hypoglycemia, risk of lactic acidosis, dc >48h preop

134
Q

Sulfonylureas key facts

A

Avoid if hypoglycemia, avoid if sulfa allergy, dc 24-48h preop

135
Q

Oral dm med that inc risk CHF

A

Thiazolinediones, end in -azone

136
Q

Which receptor stim inc v decrease insulin sec

A

Beta 2 and pns inc insulin sec. A2 stim dec insulin sec

137
Q

Very rapid acting insulin: onset, peak, duration

A

5-15 min, 45-75 min, 2-4h

138
Q

Rapid acting insulin: onset, peak, duration

A

30 min, 2-4h, 6-8h

139
Q

Intermediate acting insulin: onset, peak, duration

A

2h, 4-12h, 18-28 h

140
Q

Long acting insulin: onset, peak, duration

A

2h. 3-9h. 6-24 h

141
Q

Drugs that counter hypoglycemic effect of insulin

A

Epi, glucagon, estrogen, acth

142
Q

Drugs that extend hypoglycemic effect of insulin

A

MAOIs, salicylates, tetracycline

143
Q

Drugs to give in carcinoid crisis

A

Somatostatin (octreotide), antihistamines, 5ht3 antagonists, steroids, neo or vaso for low bp

144
Q

Drugs to avoid in carcinoid pts

A

Histamine releasers, sux, exogenous catecholamines, ephedrine, ketamine

145
Q

Levels that are inc in renal osteodystrophy

A

2 ps: phosphate and PTH

146
Q

Where each is made: angiotensinogen, ang I, ace, ang II

A

Liver, systemic circ, lung, adrenal gland

Apex Pt 2 (5 decks)

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