CMP Flashcards
1
Q
BUN: basics
A
- blood urea nitrogen
- amount of nitrogen in blood that comes from waste product urea
2
Q
BUN: what makes it high?
A
if kidneys can’t remove urea from blood normally.
- heart failure
- dehydration
- diet high in protein
3
Q
what makes BUN low?
A
liver disease or damage
2nd or 3rd trimester of pregnancy
4
Q
BUN:creatinine ratio normal range
A
usually between 10:1 and 20:1
5
Q
increased BUN:crt ratio
A
increased ratio may be due to condition that causes a decrease in blood flow to kidneys like:
-CHF
- dehydration
OR w/ increased protein from GI bleeding or increased protein in diet.
6
Q
decreased BUN:Crt ratio
A
from liver disease (due to decrease in formation of urea
or malnutrition
7
Q
what is urea?
A
waste product formed in liver when protein is metabolized into its component parts (amino acids). Process produces ammonia, which is then converted into the less toxic waste product urea.
8
Q
two of the most common causes of high blood calcium are:
A
hyperparathyroidism cancer (breakdown of bone or makes hormone similar to PTH)
9
Q
some causes of hypercalcemia:
A
hyperparathyroidism cancer hyperthyroidism sarcoidosis tuberculosis prolonged immobilization thiazide diuretics kidney transplant HIV/AIDS
10
Q
causes of hypocalcemia
A
low blood protein levels, esp. low albumin (liver disease, malnutrition, alcoholism. w/ low albumin only bound calcium is low, ionized calcium remains normal and calcium metabolism is being regulated appropriately. **most common
hypoparathyroidism inherited resistance to effects of PTH extreme deficiency in dietary calcium decreased levels vitamin D magnesium deficiency incr. levels phosphorus acute inflammation of pancreas renal failure
11
Q
Major causes of hyperkalemia
A
Increased potassium release from cells
Reduced urinary potassium excretion
12
Q
What increases potassium release from cells?
A
pseudohyperkalemia metabolic acidosis insulin deficiency, hyperglycemia, and hyperosmolality increased tissue catabolism beta blockers exercise hyperkalemic periodic paralysis Other -overdose of digitalis or related digitalis glycosides - red cell transfusion - succinylcholine -arginine hydrochloride - activators of ATP-dependent potassium channels (eg, calcineurin inhibitors, diazoxide, minoxidil, and some volatile anesthetics)
13
Q
What causes reduced urinary potassium excretion?
A
reduced aldosterone secretion reduced response to aldosterone reduced distal sodium and water delivery -effective arterial blood volume depletion acute and chronic kidney disease other -selective impairment in potassium secretion -gordon's syndrome -ureterojejunostomy
14
Q
persistent hyperkalemia requires ____ ___ ___ ___.
A
impaired urinary potassium excretion.
15
Q
what happens with k in metabolic acidosis?
A
as H enters the cells to be buffered, intracellular NA and K leave the cells and move into extracellular fluid, tending to raise plasma potassium concentration.
**doesn’t happen in lactic acidosis or keto acidosis bc of presence of sodium-organic anion cotransporter
16
Q
what does insulin do to K?
A
promotes K entry INTO cells –> ingesting glucose minimizes rise in serum K conc induced by concurrent K intake, and glucoses ingest alone in pts w/o diabetes modestly lowers serum K.
17
Q
what happens to K in uncontrolled diabetes setting?
A
insulin deficiency + hyperosmolality induced by hyperglycemia freq leads to hyperK even though there may be marked K depletion dt urinary losses caused by osmotic diuresis
two poss mech:
loss of cell water raises cell K conc –> gradient for K exit
friction forces bt solvent (water) and K (K gets dragged out of cell by water independent of electrochemical gradient)
18
Q
what do beta blockers do to K?
A
increased beta-2-adrenergic activity drives K into cells and lowers serum K. –> beta blockers that interfere w/ this (mostly nonselective beta blockers like propranolol and labetalol) –> increase in serum K
19
Q
what are major causes of hypoaldosteronism?
A
Reduced aldosterone production
Aldosterone resistance
20
Q
What causes reduced aldosterone production?
A
Hyporeninemic hypoaldosteronism
Angiotensin inhibitors, such as ACE inhibitors, angiotensin II receptor blockers, and direct renin inhibitors
Chronic heparin therapy (impairs aldosterone synthesis)
Primary adrenal insufficiency
Severe illness
Inheritted disorders
21
Q
What causes hyporeninemic hypoaldosteronism?
A
- renal disease, most often diabetic nephropathy
- NSAIDS
- calcineurin inhibitors
- volume expansion, as in acute glomerulonephritis
22
Q
What inherited disorders reduce aldosterone production?
A
- congenital hypoaldosteronism (21-hydroxylase deficiency and isolated hypoaldosteronism)
- pseudohypoaldosteronism type 2 (Gordon’s syndrome)
23
Q
what cause aldosterone resistance?
A
Inhibition of the epithelial sodium channel
Pseudohypoaldosteronism type 1
Voltage defects
24
Q
what inhibits the epithelial sodium channel in aldosterone resistance?
A
- potassium-sparing diuretics, such as spironolactone, eplerenone, amiloride, and triamterene
- antibiotics, trimethoprim and pentamidine
25
what cause voltage defects in aldosterone resistance?
- markedly reduced distal Na delivery
- acquired or congenital defects in Na reabsorption by the distal tubule principal cells (obstructive uropathy), SLE, and sickle cell disease
26
What defines acute kidney injury (AKI) in adults?
Kidney Disease: Improving Global Outcomes (KDIGO) guidelines:
- increase in serum creatinine by >/= 0.3 mg/dL w/in 48 hrs OR
- increase in serum creatinine to >/= 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days,
OR
- Urine volume <0.5 mL/kg/hr for six hours
27
AKI stage 1
increase in serum crt to 1.5 to 1.9 times baseline
OR
increase in serum art by >/=0.3 mg/dL
OR
reduction in urine output to <0.5 mL/kg/hr for 6 to 12 hours
28
AKI stage 2
increase in serum creatinine to 2.0 to 2.9 times baseline
OR
reduction in urine output to <0.5 mL/kg/hour for >/= 12 hours
29
AKI stage 3
increase in serum creatinine to 3.0 times baseline
OR
increase in serum creatinine to >/=4.0 mg/dL
OR
reduction in UOP to <0.3 mL/kg/hr for >/= 24 hours
OR
anuria for >/= 12 hours
OR
initiation of renal replacement therapy
OR
in patients < 18yrs, dear in eGFR to <35 mL/min/1.73m^2
30
causes of prerenal disease
```
hypovolemic states
alterations in renal vascular autoregulation
angiotensin blockade (ACE or ARB meds)
```
31
what cause renal hypovolemic states?
- acute hemorrhage
- diarrhea
- unreplenished insensible losses
- low effective circulating (arterial) volume such as severe systolic heart failure w/ reduced EF (cardiorenal syndrome) or acutely decompensated liver disease with portal hypertension (hepatorenal syndrome)
32
what cause alterations in renal vasculature autoregulation?
afferent arteriole vasoconstriction caused by NSAIDS or iodinated radio contrast media
33
what are causes of intrinsic renal vascular disease?
small vessel vasculitides
| diseases that cause microcangiopathy and hemolytic anemia
34
what diseases cause microangiopathy and hemolytic anemia (MAHA)?
- thrombotic thrombocytopenia purport - hemolytic uremic syndrome (TTP/HUS)
- scleroderma
- atheroembolic disease
- malignant hypertension
35
what diseases affect larger vessels and cause renal disease?
renal infarct from aortic dissection
systemic thromboembolism
renal artery abnormality (such as aneurysm)
acute renal vein thrombosis
36
causes of intrinsic glomerular disease: classification
primary (idiopathic, not assoc w/ systemic disease)
| secondary (such paraneoplastic, drug induced, or part of a systemic rheumatologist disease)
37
patterns of intrinsic glomerular disease:
```
nephritic pattern (proliferative glomerulonephritis)
nephrotic pattern (nonproliferation glomerulopathy)
```
38
what is produced in the nephritic pattern or glomerulopathy?
active urine sediment with dysmorphic red + white cells; granular, red cell, and other cellular casts; and a variable degree of proteinuria
39
what is seen in nephrotic pattern of glomerulopathy?
lots of protein
40
intrinsic tubular and interstitial disease causing AKI
most commonly is ATN from ischemia or a nephrotoxic exposure
| --> may occur following concurrent use of ACEi/ARB medications with NSAIDs or radio contrast media
41
post renal disease (obstructive uropathy): where does it occur?
Anywhere in the urinary tract.
42
what do NSAIDs do?
inhibit COX1 and COX2
43
what do COX1 and COX2 do?
convert arachidonic acid to prostaglandin
44
immediate action for patient with hyperbilirubinemia and suspected liver disease?
```
Tests:
- bilirubin fractions (direct, indirect)
- liver biochemical tests (all phos, AST, ALT
- prothrombin time / INR
- albumin
- CBC with diff and platelet count
Obtain:
-blood culture as appropriate
- RUQ imaging
```
45
immediate action for patient with hyperbilirubinemia and suspected hemolytic anemia?
tests:
- CBC with diff, platelet count, corrected or absolute reticulocyte count
- lactate dehydrogenase, haptoglobin
- peripheral blood smear
Consider:
- hematologic consult to guide eval + management of new onset hemolysis
46
what causes an elevated indirect bilirubin?
increase in unconjugated bilirubin results from bilirubin overproduction (eg hemolysis) or impairment of uptake or conjugation of bilirubin (eg Gilbert syndrome)
47
what does a predominant alk phos elevation out of proportion to AST/ALT?
suggests cholestasis in setting of extra hepatic biliary obstruction or intrahepatic cholestasis. both fractions of bilirubin usually elevated.
48
Predominant aminotransferase (AST/ALT) elevation suggests...?
disproportionate elevation in AST/ALT compared w/ alk phos suggest hepatocellular disease/injury. Both fractions of bilirubin usually elevated.
49
differential for predominant aminotransferase elevation
```
broad categories:
neoplasms
metabolic/hereditary
systemic (ex: ischemic hepatitis)
infections (ex: viral hepatitis)
toxic/immunologic (ex: hepatotoxicity from drugs or toxins,
alcoholic liver disease)
```
50
tests for persistently elevated transaminases:
- serology for viral hepatitis
- measure antimitochondrial antibodies (for primary biliary cholangitis)
- measure antinuclear, antimitochondrial, and anti smooth -muscle antibodies, and either serum protein electrophoresis or quant immunoglobulin analysis (for autoimmune hepatitis)
- serum levels of iron, transferrin, and ferritin (for hemochromatosis)
- TSH
- antibody screening for celiac disease
51
causes of unconjugated hyperbilirubinemia
- increased bilirubin production
- impaired hepatic bilirubin uptake
- impaired bilirubin conjugation
52
what causes increased bilirubin production?
```
extravascular hemolysis
extravasation of blood into tissues
intravascular hemolysis
dyserythropoiesis
Wilson disease
```
53
what causes impaired hepatic bilirubin uptake?
heart failure
portosystemic shunts
some patients with Gilbert syndrome
Certain drugs - rifampin, probenecid, flavaspadic acid, bunmiodyl
54
what causes impaired bilirubin conjugation?
```
Crigler-Najjar syndrome types I and II
Gilbert syndrome
Neonates
Hyperthyroidism
Ethinyl estradiol
liver diseases - chronic hepatitis, advanced cirrhosis
```
55
what causes conjugated hyperbilirubinemia?
Defect of canalicular organic anion transport
Defect of sinusoidal reuptake of conjugated bilirubin
Extrahepatic cholestasis (biliary obstruction)
Intrahepatic cholestatis
56
what causes defect of canalicular organic anion transport?
Dubin-Johnson syndrome
57
what causes defect of sinusoidal reuptake of conjugated bilirubin?
Rotor syndrome
58
what causes extra hepatic cholestasis (biliary obstruction)?
choledocholithiasis
intrinsic and extrinsic tumors (eg, cholangiocarcinoma, pancreatic cancer)
primary sclerosis cholangitis
AIDS cholangiopathy
Acute and chronic pancreatitis
strictures after invasive procedures
certain parasitic infections (eg, Ascaris lumbricoides, liver flukes)
59
what causes intrahepatic cholestasis?
```
Viral hepatitis
Alcoholic hepatitis
Nonalcoholic steatohepatitis
Chronic hapatitis
Primary biliary cholangitis
Drugs and toxins
Sepsis and hypo perfusion states
Infiltrative diseases (eg amyloidosis, lymphoma, Sarcoidosis, tuberculosis)
Total parenteral nutrition
Postoperative cholestasis
Following organ transplantation
Hepatic crisis in sickle cell disease
Pregnancy
End-stage liver disease
```
60
Is a VBG comparable to an ABG?
Values are reasonably comparable EXCEPT in the cases of O2 and CO2.
61
Hydrogen ions are excreted via ____.
Kidneys
62
Carbon dioxide is excreted via _____.
Lungs
63
If the buffers and excretion mechanisms are overwhelmed and acid is continually produced the pH _____. This creates _____.
Falls, metabolic acidosis
64
If the ability to excrete CO2 is compromised this creates a ______.
Respiratory acidosis.
65
What is base excess?
The amount of strong base which would need to be added or subtracted from a substance in order to return the pH to normal (7.40).
66
A base excess of more than +2 mEq/L indicates a _____.
Metabolic alkalosis
67
A base excess less than -2 mEq/L indicates a ______.
Metabolic acidosis.
68
Bicarbonate is produced by the ____.
Kidneys
69
Normal range for bicarbonate
22 - 26 mmol/L
70
If there are additional acids in the blood the level of bicarbonate will ____ as ions are used to _______.
Fall, buffer these acids.
71
What happens if there is a chronic acidosis?
Kidneys make more bicarbonate to keep pH in range.
72
What is lactate?
A by-product of anaerobic respiration
73
What raises lactate?
Any process that causes tissue to use anaerobic respiration; good indicator of poor tissue perfusion.
74
What is methaemoglobin?
Oxidized form of hemoglobin
| Levels >2 abnormal, suggest methaemoglobinaemia —> errors of metabolism, exposure to toxins like nitrates
75
Type 1 respiratory failure
PaO2 < 8 and PaCO2 low or normal
Caused by pathological process that —> lungs that can’t exchange oxygen; doesn’t change lung’s ability to excrete CO2
Ex: PE, PNA, asthma, pulmonary edema
76
Type 2 respiratory failure
PaO2 <8 and raised PaCO2
| Problem with the lungs or with mechanics / control of respiration.
77
Examples of Type 2 respiratory failure
Pulmonary problems:
- COPD
- Pulmonary edema
- PNA
```
MEchanical problems:
Chest wall trauma
Muscular dystrophies
Motor neuron disease
Myasthenia Gravis
```
Central problems:
Opiate overdose
Acute CNS disease
78
Mechanism of respiratory acidosis
Alveolar hyperventilation —> CO2 retention
79
Common causes of respiratory acidosis
Airway obstruction: COPD exacerbation, bronchial asthma
Respiratory muscle weakness
CNS depression: head trauma, post-octal state, drug toxicity (opiates, barbiturates, and benzodiazepines)
80
Respiratory acidosis pH
Decreased
81
Respiratory acidosis pCO2
Increased
82
Respiratory acidosis HCO3
Increased (compensation)
83
Respiratory alkalosis mechanism
Increase in respiratory rate and/or tidal volume —> alveolar hyperventilation —> CO2 washout
84
Common causes of respiratory alkalosis
Pain, anxiety, panic attacks
Pregnancy
High altitude
Drug toxicity (theophylline, progesterone, salicylate toxicity)
Hyperventilation while on mechanical ventilation
85
Drug toxicities that cause respiratory alkalosis
Theophylline
Progesterone
Salicylate toxicity
86
Respiratory alkalosis pH
Increased
87
Respiratory alkalosis pCO2
Decreased
88
Respiratory alkalosis HCO3
Decreased (compensation)
89
Metabolic acidosis mechanism
Increased production/ingestion of H+ or loss of HCO3-
90
Common causes of metabolic acidosis
High anion gap metabolic acidosis
| Normal anion gap metabolic acidosis
91
Causes of high anion gap metabolic acidosis
Lactic acidosis: severe tissue hypoxia, liver failure, metformin use
Ketoacidosis: diabetes mellitus, starvation, alcoholism
Renal insufficiency, uremia
Accumulation of exogenous organic acids (methanol, ethylene glycol, toluene, salicylate toxicity)
92
Common causes of normal anion gap metabolic acidosis
Renal tubular acidosis
| GI loss of HCO3- (eg diarrhea, GI fistula, intestinal stoma)
93
Metabolic acidosis pH
Decreased
94
Metabolic acidosis pCO2
Decreased (compensation)
95
Metabolic acidosis HCO3-
Decreased
96
Metabolic alkalosis mechanisms
Loss of H+ or incr production/ingestion of HCO3-
97
Common causes of metabolic alkalosis
Chloride-responsive (urinary chloride normal [<25 mmol/L
- vomiting or nasogastric suction
- hypovolemia (contraction alkalosis)
- loop or thiazides diuretics
Chloride-resistant (urinary chloride elevated [ >40 mmol/L])
- hyperaldosteronism
- Cushing syndrome
- Bartter syndrome
- Gitelman syndrome
- Liddell syndrome
98
Metabolic alkalosis pH
Increased
99
Metabolic alkalosis pCO2
Increased (compensation)
100
Metabolic alkalosis HCO3-
Increased
101
Anion gap
= difference between concentration of unmeasured anions and the concentration of unmeasured cations
