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PAM Semester 2 > Clinical Medicine Exam 4 Renal > Flashcards

Clinical Medicine Exam 4 Renal Flashcards

1
Q

Respiratory Acidosis (general)

A

ineffective breathing high co2 low ph

Acute: ETOH,CNS depress, Barb, opioid OD
Status asthmaticus, mechanical hypoventilation, ARDS

Chronic: COPD, obesity, Hypoventilation, apnea, neuromuscular disorders

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2
Q

Respiratory alkalosis (general)

A

fast deep breathing, low co2 high ph

Hyperventilation, anxiety, fear, pain

If hypoxic, PE, altitude, anemia, pregnancy

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3
Q

Metabolic acidosis (general) (+anion gap)

A

low bicarb retention, low serum bicarb, low ph

MUDPILERS CAT

(CO, cyanide, aminoglycosides, toluene)

AG= NA+ (CL-HCO3)

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4
Q

metabolic alkalosis (general)

A

Rare

increase bicarb absorption, high serum bicarb, high ph

Causes = Drugs, thiazide/loop, PCN, Bicarb

S/S= Vomiting, suction/gastric, mineralocorticoid excess

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5
Q

Metabolic acidosis General (normal anion gap)

A

Diarrhea, renal tubular acidosis, Addison’s

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6
Q

Anion gap Calc

A

Na - (Cl + HCO3) = AG

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7
Q

Urine Anion Gap

A

K + NA - CL

basic idea of ammonia excretion

loss of base through GI from diarrhea causes acidosis
this causes a negative urine anion gap

Renal tubular acidosis causes a positive urine anion gap

Not useful in metabolic acidosis with anion gap due to other solutes

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8
Q

safest route of postassium

A

oral

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9
Q

3 steps of hyperkalemia

A

protect the heart
redistribute
excrete potassium

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10
Q

Most common cause of hypocalcemia

A

advanced CKD due to decreased vitamin D3

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11
Q

Treatment of choice for hypercalcemia with malignancy

A

bisphosphonates,

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12
Q

Thiazide diuretics and hypercalcemia

A

thiazide diuretics stop calcium excretion

don’t use in hypercalcemia

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13
Q

Most common cause of hyperphosphatemia

A

Advanced

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14
Q

Stone diagnostics

A

The “gold standard” diagnostic test is helical CT without contrast

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15
Q

Calcium Stones

UA results

A

Calcium Stones

higher urine calcium
higher urine oxalate
lower urine citrate

Higher urine phosphate levels and higher urine pH

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16
Q

Uric Acid Stone

UA results

A

Low urine pH
High uric acid
pH is the predominant influence on uric acid solubility

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17
Q

Vaccines for CKD

A 
Covid -19
Flu
TDAP
Pneumo
Hep B
Zoster
HPV
MMR
Varicella
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18
Q

SIADH

A

Syndrome of inappropriate antidiuretic hormone

too much ADH

Retain too much water
Hypervolemic

hyponatremic/serum osmo/hypotonic/isovolemic/urine osmo

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19
Q

SIADH Causes

A

malignancy, pulmonary disorders, CNS disorders, medications

Hyponatremia / Hypervolemia

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20
Q

SIADH Treatment

A

fluid restriction, hypertonic saline

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21
Q

ADH

A

Produced in the hypothalamus, released by the pituitary gland

Antidiuretic hormone

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22
Q

Most common cause of signs and symptoms of too much ADH

A

Low sodium

Hyponatremia

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23
Q

Dialysis indications

A 
AKI (short term)
ESRD stage 5
PKD (10% of pts have PKD)
RCC
Hypercalcemia
Hyperphosphatemia
Hypermagnesemia
Uremia
Hyponatremia (special cases)
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24
Q

Dialysis Risks

A

Hemodialysis
need access = shunt / port / fistula / graft
high risk of infection

peritoneal dialysis
risk for peritonitis

Very elderly don’t do well

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25
Q

Dialysis Types

A

Hemodialysis
3 times a week 3-5 hrs

peritoneal dialysis
(CAPD) four to six times a day manually
(CCPD) Cycles contiguously at night

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26
Q

ESRD Defenition

A

70% are due to Diabetes & HTN/CVD

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27
Q

ESRD Stages

A

Stage 5
Kidney failure
GFR less than 15
Albuminuria 4+

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28
Q

ESRD treatment

A

Dialysis

Transplant

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29
Q

Acute glomerulonephritis ESRD

A

Acute glomerulonephritis (rapid progression, ESRD in months)

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30
Q

CKD ESRD

A

Classic urine sediment finding in ESRD – waxy casts.

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31
Q

PKD ESRD

A

10% of ESRD
50% develop ESRD by age 60
Vasopressin stimulate cystogenesis which leads to ESRD

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32
Q

ESRD Risks

A

Babies born to mothers in ESRD have a mortality rate of nearly 50%

33
Q

Hyperphosphatemia ESRP

A

Most common cause is ESRD

34
Q

Ace / Arb in Nephrotic Syndrome

A

Tx includes Ace / Arb (also statin, loop, thiazide, GC steroids)

35
Q

Ace / Arb in AKI

A

ACE inhibitors, ARBs causing efferent arteriole dilation

36
Q

Ace / Arb in Acute glomerulonephritis

A

IgA nephropathy – ACE inhibitors, (maybe corticosteroids)

37
Q

Ace / ARB in Renovascular HTN

A

If AKI occurs after initiation of ACE-I suspect RVHTN

Medical mngt – ACE-I or ARBs. BUT – both are contraindicated if bilateral stenosis present or if the patient has only 1 kidney!

38
Q

Ace / ARB in Renovascular HTN

A

If AKI occurs after initiation of ACE-I suspect RVHTN

Medical mngt – ACE-I or ARBs. BUT – both are contraindicated if bilateral stenosis present or if the patient has only 1 kidney!

Suspect RVHTN if There is an abrupt increase of more than 25% in level of serum creatinine after admin of ACE inhibitors

39
Q

Ace / ARB in CKD

A

HTN – ACE-I or ARBs – do this early in disease!

Proteinuria – same – ACE-I or ARBs – early

40
Q

What do ACE inhibitors do?

A

ACEinhibitors effectively reduce systemic vascular resistance inpatientswith hypertension, heartfailureorchronic renal disease

an important part of theirlong termrenoprotective effects inpatientswith diabetic and non-diabeticrenal disease

41
Q

When ACE / ARB are used together

A

The reduction in proteinuria appears to be greater

42
Q

ACE /ARB in PKD

A

Single, simple cyst – observe, follow up evaluation, ACE inhibitor, ARB if HTN

HTN – 50% will be hypertensive on presentation. Cyst-induced ischemia appears to cause activation of the renin-angiotensin system. Use an ACE inhibitor or an ARB

43
Q

ACE /ARB in Hyperkalemia

A

Causes – ACE inhibitors, angiotensin-receptor blockers,

(potassium-sparing diuretics, or the combination, mineralocorticoid deficiency or CKD, genetic disorders, urinary tract obstruction)

ACE inhibitors, ARBs and spironolactone, potassium-sparing diuretics should be used cautiously in patients with heart and/or liver failure and kidney disease

44
Q

ACE /ARB in Metabolic alkalosis

A

If saline unresponsive – may need surgical removal of mineralocorticoid producing tumor – if not – ACE inhibitor or Spironolactone

45
Q

AHA BP Goal

A

130/80

46
Q

GFR

A

Useful measure of kidney function at the level of the glomerulus

Measured directly via biomarkers (most commonly creatine)

Measures the amount of plasma ultrafiltered across the glomerular capillaries

Reflects the ability of the kidneys to filter fluids and various substances, including medications.

(eGFR) Estimation of Glomerular filtration rate

47
Q

GFR

A

volume of plasma filtered per unit time

Useful measure of kidney function at the level of the glomerulus

Measured directly via biomarkers (most commonly creatine)

Measures the amount of plasma ultrafiltered across the glomerular capillaries

Reflects the ability of the kidneys to filter fluids and various substances, including medications.

GFR controlled by adjusting glomerular blood pressure from moment to moment

Traditionally calculated by the creatinine clearance (requires 24 hour urine collection)

Normal values vary significantly

(eGFR) Estimation of Glomerular filtration rate

48
Q

MAP and GFR

A

Changes in MAP could impact GFR by changing Glomeular Capillary Pressure (PGC)

49
Q

GFR stability

A

Between 80 – 180 mmHg, GFR does not change much with changes in MAP because of
intrinsic regulatory mechanisms

50
Q

GFR Averages

A

Average GFR = 125 ml/min
180 L filtered daily
Only 1.5 L urine made daily
Most filtered fluid is reabsorbed

51
Q

Criteria for AKI

A

RIFLE

52
Q

Criteria for AKI

A

RIFLE

Risk, Injury, Failure, Loss, End-stage

53
Q

Most at risk for Wilms tumor

A

Most common in children under 5 years old

Most common cause of abdominal mass in children

Represents 5-6% of cancers in children younger than 15 years

54
Q

Wilms tumor Tx

A

TX – total nephrectomy plus chemotherapy

Up to 90% cure rate.

55
Q

Clinical signs of Wilms tumor

A

palpable abdominal mass does NOT cross midline,

hematuria, nausea, vomiting, HTN, anorexia – may be present.

Mass may be only clinically apparent finding

CBC usually normal, may have anemia

increasing size of abdomen or an asymptomatic abdominal mass. About 25% are hypertensive on presentation. Microscopic hematuria in approximately 25% of patients, gross hematuria is rare

56
Q

Renal Cell Carcinoma Clinical presentation

A

Tumor of the proximal convoluted renal tubule cells

highly metabolic

Renal Cell tumors are by far the most common tumor originating in the kidney (~95%)

Difficult to diagnose due to typically being asymptomatic.

Once diagnosed – difficult to treat – resistant to chemo and radiation

Most common is clear cell RCC

57
Q

RCC Risk Factors

A

smoking, obesity, dialysis, obesity, being a male (2-1), HTN, rare genetics

58
Q

Nephritic Syndrome

A

Post infectious: MCC = Strep throat, skin infections
Wegner’s granulomatosis, polyarteritis nodosa
Goodpasture’s syndrome, neuropathy, purpura

Nephritic is always associated with hypertension

proteinuria less than 3.5 g/day

Tx = Steroids

59
Q

Nephritic Syndrome

A

Post infectious: MCC = Strep throat, skin infections
Wegner’s granulomatosis, polyarteritis nodosa
Goodpasture’s syndrome, neuropathy, purpura

Nephritic is always associated with hypertension

proteinuria less than 3.5 g/day

Tx = Steroids

60
Q

Nephrotic Syndrome

A

Proteinuria > 3.5g/DAY

Most common in children

Focal segment glomerulosclerosis” – HIV, heroin, HTN

African American patients

Hypoalbunemia
Hypercholesterolemia
edema

Doesn’t cause hypertension

Tx
glucocorticoids (SLE or MCD), loop or thiazide diuretics, ACE or ARB, statin

61
Q

Nephritic syndrome and glomerulonephritis

A

Less extra, more benign, when severe it is termed rapidly progressive glomerulonephritis

Nephritic syndromeandacute glomerulonephritis.Glomerulonephritisrefers to a number of kidney problems that involve inflammation in the glomeruli, which are the kidney’s filtration units.Acute glomerulonephritiscan causenephritic syndrome.

62
Q

AKI intrinsic

Acute Glomerulonephritis

A

Intrinsic Kidney Injury (AKI)

Several etiologies – post-infection (think strep)

Tx: All forms except the rapidly progressive forms are typically self-limiting
(rapid or progressing disease = steroids/cyclophosphamide)

Edema, HTN, hypervolemia – Loop diuretics, beta-blockers, CCBs

Post strep AGN- maybe antibiotics (PEN G)

Protein + hematuria with acanthocytes + red blood cells casts – highly suggestive of glomerulonephritis
(RBC Casts)

63
Q

Hydronephrosis

A

Not a disease

ALWAYS caused by obstruction (renal calculi, BPH, neoplasm)

quite rare

UA usually neg, might have increase creatinine

Ultrasound

– usually asymptomatic – may notice change in urinary output, may be hypertensive

TX – remove obstruction

Meds – adults with hydronephrosis, complicated by infection – should be treated with abx for 3-4 weeks

Hydronephrosis with infection is a urologic emergency – treated by prompt drainage using retrograde stent insertion or percutaneous nephrostomy

64
Q

AKI intrinsic

Acute tubular necrosis

A

Most common type of AKI

Acute destruction and necrosis of the renal tubules of the nephron

endogenous nephrotoxins or prolonged prerenal azotemia

If due to prerenal azotemia – often present hypotensive and/or hypovolemic

Exogenous toxic Causes:
dye, Vanco, aminoglycosides, NSAIDS

Endogenous causes:
Tumors, cancer, Rhabdo

Urinalysis - ”Muddy Brown Casts”,

TX – first – IV fluids and remove offending agent(s)

UA = BUN 10-15:1
Urine osmo: 300
Urine Na: >40
FENA >2%

65
Q

AKI Pre renal

A

poor perfusion

BUN: creatinine ratio > 20:1

TX – replace volume

66
Q

When is BUN: Creatinine ratio reliable?

A

When not pulled from a heparin line

67
Q

AKI Post renal

A

Rare
Always obstructive

Causes BPH, BOO, Tumors, stones/strictures

BUN Creatinine ratio 10:1

usually asymptomatic

Ultrasound

TX remove obstruction

68
Q

AKI Intrinsic

A

Acute interstitial nephritis
Acute tubular necrosis
Acute glomerulonephritis

Normal BUN creatinine ration 10-15:1

69
Q

AKI Intrinsic

Acute interstitial nephritis

A

inflammatory response in the interstitium

most common cause is drug hypersensitivity (70%)

drug causes: SCCRAP
also infection, auto immune, unknown

Fever, arthralgia, rash, eosinophils

Tx remove offending agent
(usually a spontaneous recovery)

normal kidney function back in one year

70
Q

PKD

A

Adult onset

autosomal dominant disorder
Most common hereditary kidney disease

Autosomal recessive in infants

multi system

Abdominal pain, flank pain, nocturia, berry aneurysm, mitral valve prolapse

large palpable kidneys, HTN, protein/blood in urine

Ultrasound, genetic testing

simple single cyst - follow up ACE/ARB if HTN

Fluids, control HTN, treat UTI’s (preserve renal function

ESRD = dialysis / transplant

10% of ESRD
50% develop ESRD by age 60
Vasopressin stimulate cystogenesis which leads to ESRD

71
Q

Renal vascular disease

A

Renal vascular hypertension
Large vessel atherosclerosis, muscular diseases, embolotic disorders, inflammation,

blood supply changes are followed by fibrosis and loss of kidney function

72
Q

Horseshoe kidney

A

1 in 1000 have some sort of fusion
(most common is horseshoe kidney)

always contains 2 ureters

may have alternate blood supply

73
Q

Kidney biopsy

A

AGN and CKD

Nephritic syndrome

Biopsy should be considered in AKI patients with no apparent cause

Possible osteodystrophy (brown hemosiderin (cystic brown tumor)

74
Q

Kidney Imaging

A

Renal osteodystrophy = x ray

75
Q

Kidney Imaging

A

Renal osteodystrophy = x ray

Hydronephrosis = UA
(antegrade urography can be used also in AKI)

Stones = CT wo contrast, US preferred initially

small kidneys are seen with US

76
Q

Which of the following is not a cause of Hyperkalemia?

A. Rhabdomyolysis
B. K+ sparing Diuretics
C. Metabolic Alkalosis
D. Metabolic Acidosis

A

C. Metabolic Alkalosis

Rhabdo causes cell lysis
K+ is out
Both cause solute shift but Meta alk causes hypokalemia

77
Q

Of the following, which are body systems that manifest clinical signs and symptoms of hyperkalemia?

A. Neuro/muscular and Cardia
B. Cardiac and GI
C. MSK and GI
D. Neuro/muscular and GI

A

A: neuro muscular cardiac

Protect the heart

causes impaired neuromuscular junction

78
Q

What is the earliest sign of hyperkalemia on an ECG?

A. Prolonged PR interval
B. Peaked T waves
C. Widening of QRS
D. QT shortening

A

Peak T waves is early sign of hyperkalemia

QT shortening is hypercalcemia
Wide QRS is late hyperkalemia
Severe Hyperkalemia is Prolonged PR

PAM Semester 2 (22 decks)

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