Kidney, Liver, Endo Flashcards
What is in renal cortex
Glomerulus, Bowman’s capsule, proximal tubules, distal tubules
What is in renal medulla
Loops of henle and collecting ducts
What Aldosterone v adh does
Aldosterone- na and water absorbed (extracellular vol). ADH absorbs water (osmolarity).
Hormones made by the kidney
Renin, EPO, d3
Kidneys receive what % of CO. Of that what is filtered by glomerulus, what happens to other part
20-25. 20. Circulates through peritubular capillaries
Renal blood flow calc
(Map - renal venous pressure) / renal vascular resistance
Renal cortex v medulla blood flow and p50. Which area more sensitive to ischemia
Cortex= 90%, 50. Medulla= 10%, 10. Medulla more sensitive
RBF in neonate, when it achieves adult level
Doubles first 2 weeks of life. Adult level at 2 years old
How kidney autoregulates to maintain renal perfusion
When perf too low, bf inc by reducing vascular resistance. Vice versa is true
Renal blood flow autoreg range
Map 50-180
Most important methods of autoreg in kidney
Myogenic mechanism and tuboglomerular feedback
What increases renin release
Reduced renal perf, b1 activation, dec na and cl delivery to distal tubule
What things increase aldosterone release
High k, low na, RAAS stim
What controls adh release
Inc osmolarity of ECF and decreased blood vol
How adh restores bp
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
Which anesthesia related things impact adh homeostasis
Inc by peep, pos pressure vent, hypotension, bleeding
How ANP acts
Produced in myocardium in resp to atrial distension. Stim na and h20 excretion in collecting ducts. Neg feedback to RAAS, inhib renin release
DA1 v DA2
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
Calc: net filtration pressure in kidney
Glom hydrostatic p - Bowman’s capsule hydrostatic p - glomerular oncotic p
What conditions inc gfr and filtration fraction
Constriction of efferent arteriole and dec plasma protein
Most important determinant of gfr
Glomerular hydrostatic pressure
What determines glomerular hydrostatic pressure
Arterial bp, afferrent arteriolar res, efferent arteriolar res
Reabsorption
From tubule to peritubular capillaries
Secretion
From peritubular capillaries to tubule
Excretion
Removal from body in urine
Urinary excretion rate=
Filtration - reabsorption + secretion
Where is most of filtered na reabsorbed
Proximal tubule
Func of proximal tubule, what happens here
Bulk reabsorption of solutes and h20. 65% of h20, na, k, cl, and bicarb
Func of desc loop of henle
Water reabsorption, countercurrent inc osmolarity of peritubular fluid to achieve this
Ascending loop of henle function
K, na, and cl pumped into interstitium. Impermeable to h20. UF hypotonic. H excreted. Still countercurrent
Distal tubule func
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
Collecting duct func
Regulates conc of urine. ADH inc h20 reabs, anp inhib h20/na reabs. Aldosterone works here. Adjusts h conc
How CAI diuretics work
Inhib carbonic anyhydrase, reduces reabsorption of hco3, na, and water in proximal tubule
Uses of CAIs
Open angle glaucoma, high altitude sickness, central sleep apnea
Complic of CAIs
Metabolic acidosis, hypokalemia, in COPD loss of hco3 may exac cns dep from hypercarbia
How osmotic diuretics work
Inhib h20 reabsorption in proximal tubule and loop of henle. They pull ECF into IV space. Good for brain bad for heart
Uses of osmotic diuretics
Prevent AKI, ic htn, dx acute oliguria (inc UOP if prerenal)
Complic of osmotic diuretics
CHF, pulm edema, if bbb disrupted will enter brain and cause cerebral edema
How loop diuretics work
Poisons na k 2cl transporter, lose dilute urine, k, ca, mg, and cl
Complic of loop diuretics
Hypochloremic metab alkalosis, pot nmbs, weakness, ototoxic, reduced lithium clearance
How thiazide diuretics work
Inhib na cl transporter in distal tubule. Inc serum ca and can inc bg
Complic of thiazide diuretics
High bg/ca/uric acid, low k, metab alkalosis, HLD
K sparing diuretics moa
Amigo ride and triad inhib k sec and na reabs in CD. Spironolactone = aldosterone antag, inhib k sec and na reabs in CD
Complic of k sparing diuretics
High k (inc if using nsaids/bb/ace inhib), metab acid, gynecomastia, libido changes, nephrolithiasis
Best tests of tubular func
Frac exc of na and urine osmolality
Tests of GFR
BUN and creatinine clearance
Bun <8 means what
Overhydration, dec urea produc (malnutrition or liver dis)
Bun 20-40 means what
Dehyd, inc protein input (diet, GIB, hematoma breakdown), catabolism (sepsis or trauma), dec gfr
100% inc in creatinine means what
50% reduction in gfr
Nml bun to creat ratio. If >20:1= what
10:1. If >= azotemia.
GFR calc
((140-age) x (kg)/(72 x creat)
Fe(na) <1% means what
More na conserved than creat cleared. = prerenal azotemia
If Fe na >3% means what
More na excreted than creat cleared. Means tubular func impaired
Prerenal oliguria looks like what w tests
Fe na <1, urinary na <20, osmolality of urine >500, ratio >20:1, nml sediment or maybe hyaline casts
Acute tubular necrosis looks like what in tests
Fe na >3, urinary na >20, urine osmolality <400, bun cr ratio normal. Tubular epithelial casts or granular casts
Uremic bleeding: cause, what is normal, tx
Dysfunctional platelets. Normal pt, ptt, and plt count. Tx is desmopressin, dialysis preop
Prop in renal pts dose and why
Inc dose, hyperdynamic circ and bbb disrup d/t uremia
Precedex use in renal pts
Liver metab, safe to use. Doa may be prolonged
Preventative strategies for contrast media induced AKI
Nacl, low/isoosmolar contrast, sodium bicarb
SE and use of calcineurin inhib in renal pts
Immunosuppression for transplants. SE: htn, renal vasoconstriction
Turp: level required for spinal. Resec time limit and solution height above table
T10. 1 hr or less. <30 cm above table
Turp solution pro and SE: distilled water
Good for surgeon. Inc risk turp syndrome, dec, na, hemolysis, hemoglobinuria
Turp solution pro and SE: glycine
Dec risk turp syndrome. Inc ammonia, dec loc, postop blindness
Turp solution pro and SE: sorbitol
Dec risk turp syndrome. Hyperglycemia, lactic acidosis
Turp solution pro and SE: mannitol
Osmolarity similar to plasma, no renal metab. Transient plasma expansion —> risk if lv fail
Turp solution pro and SE: NACL
Absent of many se. Can only be used if bipolar cautery, cant use unipolar (current)
Turp syndrome: triad, na level <120, na level <110
Hypertension (inc PP), bradycardia (reflex), alt LOC. <120= inc risk complic. <110 sz, coma, lethal ventric dysrhythmias
Absolute contraindications to ESWL
Pregnancy, bleeding disorders, anticoagulation
What removes bacteria from liver
Kuppfer cells
Liver version: arterioles, capillaries, venule s
Term branches of hepatic a and portal v. Sinusoids. Central vein
In liver, which zone best oxygenated, which worst oxygenated, which has highest conc of cp450 enzymes
Best= zone 1 (periphery). Worst= zone 3 (near central vein)). Highest cp450, zone 3
Liver: % of CO, blood flow to liver
- Aorta to sphlanchnic to portal v to liver. Or aorta to hep artery to liver
Portal vein: ___% of liver bf, ____% of o2 content
75% bf, 50% constant (lower o2 sat)
Hep artery: __% bf to liver, ___% 02 content
25, 50 (higher constant)
Portal htn dx: portal vein p, sinusoidal p
> 20, >5
Hepatic artery perf p calc
MAP - hepatic vein pressure
Hepatic arterial buffer response. What happens, what mediates it, what impairs it
Reduc in portal v flow compens by inc hepatic artery flow. Mediated by adenosine, impaired by severe liver disease
Effect of anesthesia on hepatic BF
Dec MAP, can reduce hepatic bf 30-50%
Procoagulants made by liver
Thrombopoietin, alpha 1 glycoprotein, factor 7
Factor VIII is made in the _____ but not made by the _____
Made in liver. Not made by hepatocytes
Albumin= reservoir for ____ drugs
A1 glycoprotein= reservoir for ____ drugs
Acidic. Basic
AST/ALT ratio > ___ suggests cirrhosis or etoh liver disease
2
most sensitive indicator of biliary duct obstruction
5 nucleotidase
Bilirubin levels if damage: before liver, in liver, after live (cholestatic)
Before= inc unconjugated. In or after= inc conjugated
Markers of hepatitis a
IgM early, IgG late
IA that makes most trifluoroacetic acid, IA doesnt make any
Halothane. Sevo makes none
RF for IA induced TFA/hepatitis
> 40 years old, female, >2 exposures, genetics, obesity, CYP2EI induction (etoh, isoniazid, phenobarb)
Hepatitis: most common cause, 2nd most common. Dx of it
Etoh. Hep c. Inc liver enzymes, bilirubin, cell changes
S/sx and lab changes w hepatitis
Jaundice, fatigue, low plt, glomerulonephritis, neuropathy, arthritis, myocarditis. Pt prolonged, dec albumin
Anes consid to maintain hepatic bf
Use iso (preserves it), avoid peep (inc resistance to drainage), normocapnia, liberal IVF, regional ok if no coag alt
Hepatotoxic drugs that inhib cyp 450
Tye, amio, halothane, abx (pcn, tetracycline, sulfonamides)
Etoh withdrawal syndrome: when s/s appear, peak. Early and late s/s
Appear 6-8 hr. Peak 24-36 hr. Early: tremor, halluc, nightmares. Late: inc sns (hi hr and bp, dysrhythmias), Nv, insomnia, agit
Tx etoh withdrawal
Etoh, BB, A2 agonists
When DTs occur. S/s. Tx
2-4 days after no etoh. Grand mal sz, hi hr, hi or low bp, combative. Valium or benzos, BBs
Tx drug for alcoholics in recovery. SE of it
Disulfiram. Hepatotoxic. Inhib dopa beta hydrozylase —> hypotension
MELD: what it assesses. Low risk, high risk
Bilirubin, INR, and serum creatinine. <10. >15
Child Pugh score: what it assesses, classes
Albumin, PT, bilirubin, ascites, encephalopathy. A= 10% risk periop morbid. B= 30. C= 80
Child Pugh score: how class scoring impacts proceeding to surgery
A or B ok to surgery if optimized. C should be medically managed until function improves (hepatic)
Drugs that relax sphincter of oddi
Glucagon, glyco, atropine, narcan, ntg
Ant pituitary hormones
Fsh, lh, acth, tsh, prolactin, growth hormone
T3 compared to T4
T3 has higher potency and shorter half life
T3 is a ____hormone, T4 is a ____hormone
T3= prohormone. T4= active hormone
Hypothyroid: lab alt, what causes goiter
Tsh chronically high. Thyroglobulin colloid causes gland to inc since tsh high
How thyroid hormones effects heart
Inc contractility/rate/rate of relaxation, dec SVR
How thyroid hormone effects resp and mac
Inc co2 produc __> inc vt and rr. No effect on mac. Dec rate of induc
Effect of k iodide on hyperthyroidism
Reduces thyroid hormone synthesis and release, given 10d preop
Drugs that inhib conversion of t4 to T3
Propranolol, esmolol, ptu, methimazole, carbimazole
If emergent thyroid sx give what rx
Bb, k iodide, glucocorticoid, ptu
Avoid what in thyroid surgery
Sympathomimetics, anticholinergics, ketamine, panc
What thyroid storm can mimic under GA
MH, pheo, neuroleptic malignant syndrome, light anesthesia
What Block’s thyroid synthesis
Methimazole, ptu, k iodide
What Block’s thyroid release
Iodine/iodide
Why aspirin bad in thyroid pt
Dislodges t4 from plasma proteins and inc free frac of t4
Signs of hypocalcemia
Spasms, tetany, laryngospasm, mental status alt, low bp, prolonged qt, parasthesias, chvosteks and trousseaus
Hypothyroid: rx given and initial response
T4, natiuresis and dec tsh
Induction (inhalation) is ____ w hypothyroid
Faster
Hormones made in: zona glomerulosa, fasciculata, reticularis
Mineralcorticoids, glucocorticoids, androgens
How to remember what adrenal cortex zones release
Salt, sugar, sex
Aldosterone causes what shifts
Na and h20 reabsorption. K and h excretion
Aldosterone release is inc by what 3 things
RAAS activ, high k, low na
Aldosterone regulates what, does not regulate what. Causes metabolic ___
Reg iv vol not osmolarity or na conc. Alkalosis
What doesnt have glucocorticoid effects
Aldosterone
What doesnt have mineralcorticoid effects
Decadron, betamethasone, triamcinolone
Conns disease: excess ____. Features, anes implic, tx
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)
Cushings: k shift, metabolic ___, anes implic
Low k, alkalosis. Post op give steroid. May have DI after resection
Signs of adrenal insuff
Low k, hi na, metab acid, low bg and bp, nv
When pt should get stress dose of steroids preop
> 20 mg/day prednisone (80 hydrocortisone) for over 3 weeks
Hydrocortisone if minor, moderate, or major sx
Minor: 25 mg. Moderate: 50-75 mg. Major: 100-150
Hormone released by pancreatic cells: alpha, beta, delta
Glucagon, insulin, somatostatin
Drugs that inc or dec blood glucose
Inc by beta agonists. Dec by BB or VAs
What stim v inhib glucagon release
Stim: decreased glucose, stress, sepsis, trauma, b agonist. Inhib: inc glucose, insulin, somatostatin
What somatostatin does
Inhibits insulin and glucagon. Dec sphlanchnic bf and dec motility
Biguanides (metformin): key facts/risks
Doesn’t cause hypoglycemia, risk of lactic acidosis, dc >48h preop
Sulfonylureas key facts
Avoid if hypoglycemia, avoid if sulfa allergy, dc 24-48h preop
Oral dm med that inc risk CHF
Thiazolinediones, end in -azone
Which receptor stim inc v decrease insulin sec
Beta 2 and pns inc insulin sec. A2 stim dec insulin sec
Very rapid acting insulin: onset, peak, duration
5-15 min, 45-75 min, 2-4h
Rapid acting insulin: onset, peak, duration
30 min, 2-4h, 6-8h
Intermediate acting insulin: onset, peak, duration
2h, 4-12h, 18-28 h
Long acting insulin: onset, peak, duration
2h. 3-9h. 6-24 h
Drugs that counter hypoglycemic effect of insulin
Epi, glucagon, estrogen, acth
Drugs that extend hypoglycemic effect of insulin
MAOIs, salicylates, tetracycline
Drugs to give in carcinoid crisis
Somatostatin (octreotide), antihistamines, 5ht3 antagonists, steroids, neo or vaso for low bp
Drugs to avoid in carcinoid pts
Histamine releasers, sux, exogenous catecholamines, ephedrine, ketamine
Levels that are inc in renal osteodystrophy
2 ps: phosphate and PTH
Where each is made: angiotensinogen, ang I, ace, ang II
Liver, systemic circ, lung, adrenal gland
