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Clin Med 2 > Exam 6 > Flashcards

Exam 6 Flashcards

1
Q

Roles of kidney (3)

A

Eliminate waste
Drug metabolism/excretion
Regulate body fluids

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2
Q

3 layers of glomerular capillaries

A

Endothelium (don’t allow blood cells to pass)

Basement membrane (best barrier, allows solute and fluid to pass)

Epithelium (fenestrated foot processes, limit what filters out)

Negative charge to repel large, negatively charged molecules

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3
Q

Mesangial cells

A

Structural cells in the glomerulus, don’t participate in filtration

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4
Q

Bowman’s space

A

Filtered fluid collects here, the filtrate

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5
Q

GFR

A

Filtrate formed per minute by both kidneys combined

Depends on starling forces

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6
Q

Cockcroft fault equation

A

(140-age)/Cr, x .9 in a female

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7
Q

GFR can also be calculated from…

A

BUN or Cr

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8
Q

Main mechanism for modifying GFR?

A

Diameter of afferent and efferent arterioles

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9
Q

A positive sodium balance will…

A

Increase ECF volume

Intake>excretion

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10
Q

A negative sodium balance will…

A

Decrease ECF volume

Excretion > intake

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11
Q

Under normal conditions, almost all Na is…

A

Reabsorbed

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12
Q

Proximal convoluted tubule

A

Isosmotic reabsorption of water (and other things)

Most of Na is absorbed here

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13
Q

Thin descending limb

A

Water and sodium permeable

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14
Q

Thin ascending limb

A

Water impermeable, but sodium permeable

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15
Q

Thick ascending limb

A

Water impermeable

Active reabosorbing of sodium

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16
Q

Countercurrent multiplication

A

Blood flows through vasa recta in opposite flow of tubule

Bottom of loop concentrates blood

Water diffuses from descending limb back into bloodstream

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17
Q

ADH effects on collecting duct

A

Up regulates aquaporin channel insertion, H2O absorption

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18
Q

Polyuria, oliguria, anuria

A

Polyuria- >2500

Oliguria- <500

Anuria- <50

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19
Q

Hyaline cast

A

Normal OR

Fever, concentrated urine, exercise

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20
Q

RBC casts

A

Glomerulonephritis

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21
Q

WBC casts

A

Pyelonephritis

Interstitial nephritis

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22
Q

Renal tubular cell casts

A

Acute tubular necrosis

Interstitial nephritis

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23
Q

Broad waxy casts

A

Chronic kidney disease

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24
Q

Serum sodium reference range

A

135-145

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25
Q

Serum osmolality reference range

A

285-295

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26
Q

Osmolality equation

A

2(Na) + glucose/18 + BUN/2.8

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27
Q

If spot urine is <10, suggests…

A

Extrarenal salt loss

Kidneys trying to hold onto all of the salt that they can

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28
Q

After determining volume status for hyponatremia, determine…

A

Osmolality

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29
Q

Hypotonic hypovolemic hyponatremia

Extrarenal salt loss

A

Dehydration from vomiting, diarrhea or sweating

Fluid replaced with hypotonic liquid

Free water retained to maintain intravascular volume

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30
Q

Hypotonic hypovolemic hyponatremia

Renal salt loss

A

Excess excretion of sodium into the urine

Could be diuretics, ACE inhibitors, renal tubular epithelial dz

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31
Q

Euvolemic hypotonic hyponatremia

A

Could be hormonal, like hypothyroid or adrenal insufficiency

Post op

HIV

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32
Q

ADH

A

Secreted from posterior pituitary

Released based on extracellular osm and BP- if >280 then secretion of ADH

**arterial vasoconstriction

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33
Q

SIADH

A

Euvolemic hypotonic hyponatremia

Small cell lung CA one of principal causes

Water retention stimulated natriuresis

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34
Q

SIADH presentation

A

Clinical diagnosis- hyponatremia, decreased Osm, no other diseases, >20 urine sodium

Signs of volume loss rule this out

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35
Q

Psychogenic polydipsia causes…

A

Euvolemic hypotonic hyponatremia

Excess free water intake, excretion of sodium keeps them euvolemic

Eventually the sodium will drop

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36
Q

Hypervolemic hypotonic hyponatremia

A

States of edema, such as…

HF
Cirrhosis
Nephrotic syndrome
Hypoalbuminuria
ESRD

Increased RAAS and ADH secretion

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37
Q

Isotonic hyponatremia

A

Pseudohyponatremia can result with marked excess of substance that reduces plasma volume in blood like protein or triglycerides

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38
Q

Hypertonic hyponatremia

A

Intracellular water pulled into hypertonic ECF

Mannitol administration or hyperglycemia

Something other than sodium is the osmolalite

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39
Q

Emergent hyponatremia and treatment goals

A

Acute hyponatremia with any symptoms

Rapidly increase serum sodium by 4-6 over several hours

**do not exceed 8-10 in 24 hours

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40
Q

Osmotic demyelinating syndrome

A

Overzealous correction of hyponatremia, reversible if caught early and sodium re-lowered

Mexican hat sign on CT

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41
Q

If acute, hyperacute or severe with sx, treatment…

A

IV hypertonic saline

Watch rate of rise

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42
Q

Nonemergent, chronic with minimal sx treatment…

A

Fluid restriction

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43
Q

Hypernatremics all have…

A

Hyperosmolality

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44
Q

Causes of hypernatremia

A

Free water loops

Iatrogenic

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45
Q

Manifestations of hypernatremia

A

Dehydration, tachycardia, tenting

Neuro symptoms, variable and not very different than hyponatremia

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46
Q

Hyperaldosteronism

A

Causes hypertension

Generally mild, sometimes hypokalemia

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47
Q

Osmolar diuresis

A

Diuresis due to nonabsorbed, nonelectrolyte solute (like mannitol, glucose and urea)

Water loss in excess of sodium loss

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48
Q

If urine osmolality is <250, suggests…

A

Diabetes insipidus

Dilute or low specific gravity

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49
Q

Diabetes insipidus

A

ADH deficiency or resistance

Not released with increasing Osm

Polydipsia, polyuria, hypernatremia

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50
Q

Central DI

A

Primary- autoimmune, genetic

Secondary- hypophyseal damage

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51
Q

Nephrogenic DI

A

Acquired ADH resistance

Variety of reasons

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52
Q

DI workup

A

24 hour urine volume and Cr

Desmopressin challenge- central DI patients will have reduced thirst and urination, but no change if nephrogenic

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53
Q

Potassium main driver of…

A

Cells and sets resting potential for excitable cells

Mostly inside cells

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54
Q

Insulin and sodium/potassium ATPase function

A

Pushes potassium into cells, can cause hypokalemia

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55
Q

Metabolic acidosis and potassium

A

Hyperkalemia

In an acidotic state, protons outside of the cell need to go inside, and the antiporter pushes potassium out of cells

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56
Q

Potassium mainly absorbed in…

A

Proximal convoluted tubule

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57
Q

Potassium secretion in the kidney

A

Largely in distal tubule

Insulin pushes K into cells and causes excretion

Aldosterone causes K excretion

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58
Q

Hypokalemia and excitability

A

Hyperpolarization, tougher to trigger action potential

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59
Q

Hyperkalemia and excitability

A

Depolarization, easier to trigger action potential

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60
Q

Hypokalemia general causes

A

Increased entry into cells

Increased GI losses

Increases urinary losses

Increased sweat loss

Dialysis

Plasmapheresis

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61
Q

Trauma and epinephrine will cause…

A

Hypokalemia

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62
Q

Magnesium deficiency

A

Must be considered in refractory hypokalemia!!

Mg inhibits K secretion, so decreased Mg allows greater K secretion

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63
Q

Hypokalemia and HTN?

A

Aldosterone excess

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64
Q

Severe hypokalemia symptoms

A

Paralysis
Decreased DTR
Tetany
Rhabdo

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65
Q

Hypokalemia EKG changes

A

Flattened and broadened T waves

U waves

PVTs

ST depression

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66
Q

Hyperkalemia

A

Rare

Generally not from increase intake, but an inability to excrete in the urine

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67
Q

Hyperkalemia a few causes

A

Catabolism of tissue (rhabdo)

Beta blockers

Hypoaldosteronism

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68
Q

Drugs that cause hyperkalemia

A

K sparing diuretics
ACEI/ARBs
Trimethoprim
Digitalis toxicity

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69
Q

Hyperkalemia EKG changes

A

Peaked T waves
Wide QRS
Vfib, cardiac arrest

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70
Q

Acute kidney injury definition

A

Abrupt loss of kidney function causing retention of urea and nitrogenous waste

Dysrregulation of extracellular volume and electrolytes

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71
Q

How is AKI determined?

A

By serum Cr, GFR and urine output

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72
Q

KDIGO criteria of AKI

A

Serum Cr increase of >.3 in 48 hours

Serum Cr increase of >1.5x baseline within prior 7 days

Urine volume 6 hours

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73
Q

AKI signs and symptoms

A

Uremia causes symptoms, like NV, malaise, abdominal pain

Signs- HTN, hypo or hypervolemia, electrolyte imbalances

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74
Q

If prerenal AKI, BUN:Cr is…

If ATN AKI, BUN:Cr is…

A

> 20:1

Normal

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75
Q

If ATN AKI, micro UA shows…

A

Muddy brown granular and epithelial cell casts

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76
Q

If prerenal AKI, fractional excretion of sodium is…

A

Low, <1%

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77
Q

If ATN causes AKI, fractional excretion of sodium is…

A

High, >2-3%

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78
Q

Urine osmolality in AKI with prerenal versus ATN

A

Prerenal is >500

ATN is <450

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79
Q

AKI lab findings (random)

A 
Hyperkalemia
Hyperphosphatemia
Hyperuricemia
Hypocalcemia
Anemia
Metabolic acidosis (lost the ability to buffer)
80
Q

AKI imaging

A

Should all (with unknown etiology) undergo imaging

Renal US, helical CT for stones

81
Q

Most common cause of AKI?

A

Prerenal!

Hypovolemic, decreased CO, CHF, liver failure, impaired renal autoregulation

82
Q

Prerenal AKI is caused by…

A

Renal hypoperfusion

Volume depletion, changes in vascular resistance, low cardiac output

Can result in ischemia and intrinsic injury

83
Q

NSAID effect on afferent arteriole

A

Blocks the dilation of the afferent arteriole in response to decrease of renal blood flow

84
Q

ACEI/ARB effect on efferent arteriole

A

Blocks the constriction in response to decreased renal blood flow

85
Q

Prerenal AKI labs

A

BUN:Cr >20:1

Low fractional excretion of sodium

86
Q

Prerenal AKI traetment options

A

Maintain euvolemic
Monitor potassium
Treat underlying cause

87
Q

Post renal AKI is most commonly…

A

Obstructive

BPH in men

Urinary flow blocked causing increase in intraluminal pressure, parenchyma damage

Least common

88
Q

Anticholinergic drugs and neurogenic bladder cause…

A

Postrenal AKI

89
Q

Postrenal AKI signs/symptoms

A

Abdominal pain
Anuria/polyuria
Azotemia

Enlarged prostate
Distended bladder
Mass on pelvic exam

90
Q

Later labs of postrenal AKI

A

Increase fractional urine excretion

Isosthenuria

91
Q

Isosthenuria

A

Same osmolality in the urine and the plasma because the kidneys are not concentrating/diluting the urine properly

Seen in postrenal AKI

92
Q

Eval of postrenal AKI

A

Bladder cath/US

CT or MRI

Avoid volume depletion !

93
Q

Two major causes of acute tubular necrosis

A

Ischemia (prolonged HOTN or hypoxemia)

Neophrotoxin exposure (endogenous or exogenous)

94
Q

Can’t use contrast die if the Cr >….

A

1.4

95
Q

Endogenous nephrotoxins

A

Heme products, uric acid, paraproteins

Myoglobinuria, Hb, hyperuricemia, bence jones in multiple myeloma

96
Q

Rhabdo general

A

Necrotic muscle releases large amounts of myoglobin which is freely filtered across the golmerulus

97
Q

Rhabdo causes injury to…

A

Renal tubules- direct damage from reabsorption of myoglobin

Distal tubular obstruction from casts and intrarenal vasoconstriction

98
Q

Rhabdo signs/symptoms

A

Muscular pain

Serum CK >20,000-50,000

Dark brown urine

99
Q

Rhabdo treatment

A

Volume repletion

Mannitol

100
Q

Acute tubular necrosis labs

A

BUN:Cr <20:1
Hyperkalemia
Hyperphosphatemia
Hypermagnesemia

101
Q

Urine in acute tubular necrosis

A

Urine sodium concentration >20

Muddy brown, granular renal tubular casts

102
Q

Avoid volume overload and hyperkalemia in acute tubular necrosis treatment

A

Loop diuretics

Thiazide diuretics

103
Q

Interstitial nephritis general

A

Interstitial inflammatory response with edema and tubular cell damage

Cell mediated immune reactions with T lymphocytes

104
Q

Interstitial nephritis etiologies

A

Usually drugs (even NSAIDs and PPIs)

Could be infectious or immunologic

105
Q

Clinical findings of interstitial nephritis

A

Fever
Rash
Arthralgias
Eosinophilia

106
Q

Urine in interstitial nephritis

A

RBCs in urine almost always, WBC and white cells casts

Proteinuria

Eosinophiluria

107
Q

Renal artery stenosis causes

A

Atherosclerosis almost always (especially if older than 45)

Fibromuscular dysplasia (women <40 with unexplained HTN)

108
Q

RAS clinical findings

A 
HTN at <30 years old
Severe or stage 2 HTN after 55 years old
Resistant HTN
Acute rise in BP
Bruits
109
Q

What happens in a patient with RAS that is given an ACEI or ARB?

A

Acute increase of serum Cr at least 30%

Prevents constriction of efferent arteriole, the blood flow to the kidney is already decreased so GFR decreases

110
Q

RAS imaging

A

Renal angiography is the gold standard

Beads on a string for fibromuscular dysplasia

CT angiography highly accurate for atherosclerosis but not as much for fibromuscular dysplasia

111
Q

RAS treatment

A

Angioplasty (with or without stenting)

Surgical bypass

112
Q

Renal tubular acidosis general

A

Syndrome due to defect in proximal tubule bicarb reabsorption, or defect in distal tubule hydrogen ion secretion (or both)

Results in: hyperchloremic metabolic acidosis with normal to moderately decreased GFR

113
Q

Anion gap in RTA is…

A

Normal

Bicarb decreases, but chloride increases

114
Q

Type 1 RTA

A

Distal RTA

Defective H secretion

Can’t acidify urine, renal sodium wasting

Hypokalemia

115
Q

Type 2 RTA

A

Proximal

Defective bicarb reabsorption

Inappropriately high urine pH, bicarb replaced in circulation by chloride so hyperchloremic

Hypokalemia

116
Q

CKD definition

A

Presence of kidney damage OR decreased kidney function (GFR <60) for 3 or more months regardless of cause

117
Q

CKD signs/symptoms

A

Develop slowly, nonspecific

Uremic syndrome in ESRD

118
Q

Labs in CKD

A 
Anemia
Hyperkalemia
Hyperphosphatemia
Hypocalcemia
Metabolic acidosis
119
Q

Urine in CKD

A

Broad, waxy casts
Isosthenuria
Proteinuria

120
Q

CKD imaging

A

Ultrasound

If small, CKD because they are scarred down

If normal or large, could have nephropathy, adult PCKD, etc

121
Q

Hemodialysis

A

Constant flow of patient’s blood along side of semipermeable membrane with a cleansing solution along the other

Diffusion and removal of unwanted substances in blood while adding back necessary o nes

122
Q

HD types

A

Arteriovenous fistula (preferred)- takes 6 to 8 weeks to mature, lasts longer than graft

Prosthetic graft

**time consuming

123
Q

Peritoneal dialysis

A

Peritoneal membrane is the dialyzer

Could be continuous ambulatory (4-6 x a day manually) or automated peritoneal dialysis (automatically performs exchange, usually at night)

124
Q

BP traetment goal in CKD patient

A

<130/80 with protein in urine

<140/90 with no protein in urine

125
Q

Treatment goal for urinary protein excretion in CKD

A

<1000 mg/d proteinuria

126
Q

Life expectancy of those undergoing dialysis

A

3-5 years

127
Q

CVD complications of CKD

A

80-90% of patients die of CVD before reaching dialysis

Electrolytes, oxidative stress, etc cause death

HTN is the main issue

128
Q

HTN of CKD

A

Most common complication

Salt and water retention with a high renin state

ACEI and ARBS

129
Q

CHF in CKD

A

CKD increases cardiac workload from HTN, volume overload, anemia and atherosclerosis

Can cause cardiorenal syndrome

130
Q

Pericarditis in CKD

A

Rare in uremic patients

Fever, chest pain, friction rub

131
Q

Mineral metabolism in CKD

A

Disturbances of PTH, Ca and Ph metabolism, active vitamin D

132
Q

Minerals in CKD issues

A

Bone disease
Increased fracture risk
Vascular calcification

133
Q

Renal osteodystrophy

A

Advanced CKD
Osteitis fibrosa cystica- most common

Bony pain, muscle weakness, fracture risk

134
Q

Anemia in CKD

A

Decreased EPO production

Fe deficiency

135
Q

Coagulopathy in CKD

A

Platelet dysfunction

Mildly decreased platelet count and prolonged bleeding time f

136
Q

Hyperkalemia in CKD

A

Stage 5,but earlier in type 4 RTA, acidemic state, cellular dystruction

*EKG monitoring

137
Q

Acid base in CKD

A

Metabolic acidosis due to retention of H ions

138
Q

Uremic encephalopathy in CKD

A

Develops with GFR <5-10

Nystagmus, weakness, asterixis, hyperreflexia, coma, lethargy

139
Q

Neuropathy in CKD

A

Stocking glove
Isolated or multiple isolated
Autonomic dysfunction

140
Q

Endocrine in CKD

A

Diabetics at increased risk of hypoglycemia

Lactic acidosis risk with metformin and GR <60

Women: anovulation, pregnancy can exacerbate CKD, fetal mortality with ESRD

141
Q

Nephritic syndrome general

A

Inflammatory injury or cell proliferation

Acute kidney injury

142
Q

Nephritic syndrome presentation

A

Hematuria
Proteinuria 1-3 g/d
HTN
Edema

143
Q

Gold standard for glomerular disorders ?

A

Kidney biopsy!

144
Q

More common in nephritic versus nephrotic?

A

Increased sediment
RBC
RBC casts

145
Q

Rapidly progressive glomerulonephritis general

A

Severe inflammatory, weeks to months

**crescents within bowman’s capsule that develop

146
Q

Post infectious glomerulonephritis commonly caused by…

A

Strep, staph skin infections

GABHS

Some viral, fungal and parasitic

147
Q

Presentation of postinfectious GN

A

1-3 weeks post infection
Common in young kids 2-10

Edema, Coca Cola colored urine
HTN

148
Q

Post infectious GN labs

A

ASO antibodies
RBC and RBC casts
<3 G protein

149
Q

Post infectious GN biopsy

A

Large and dense humps

Lumpy bumpy or starry sky pattern

150
Q

IgA nephropathy general

A

IgA immune complexes deposit in the mesangium

Most common glomerulonephritis in the US

151
Q

IgA nephropathy presentation

A

Children and young adults

Associated with other infection, like URI, viral illness

*gross hematuria and dark Coca Cola colored urine 1-2 days after onset of infection

152
Q

Indicator of poor prognosis in IgA nephropathy?

A

Proteinuria >1g/d

153
Q

Essential diagnostic to IgA nephropathy

A

Immunofluorescene microscopy, has both IgA and C3

154
Q

Henoch schonlein purpura general

A

Small vessel vasculitis, IgA deposition in vessel walls

Young males

155
Q

Henoch presentation

A

Inciting infection

Palpable purpura

Arthralgia

Abdominal symptoms

HTN

156
Q

Pauci-immune glomerulonephritis genearl

A

ANCA associated small vessel vasculitides, has inciting infections:

Granulomatosis with polyangiitis
Churg- Strauss
Microscopic polyagiitis

157
Q

Pauci-immune glomerulonephritis presentation

A

Fever, malaise and weight loss prodrome

Hematuria, proteinuria

Purpura

Mononeuritus

158
Q

Granulomatosis with polyangiitis

A

Sinusitis, lower respiratory tract

Can result in hemoptysis

159
Q

Pauci-immune GN diagnostics

A

ANCA subtyping

Necrosis and crescents

160
Q

Pauci-immune GN prognosis

A

Very poor without treatment

161
Q

Anti GBM GN general

A

Renal disease or combined with pulmonary hemorrhage to be Goodpasture syndrome

Autoimmune response against GBM, cross reacts with pulmonary alveolar capillary basement membranes

162
Q

Anti GBM GN presentation

A

Hemoptysis, dyspnea, respiratory failure maybe

Often after URI

Hematuria, HTN, edema

163
Q

Anti GBM GN biopsy

A

Crescents

Ribbon like on immunofluorescence

164
Q

Cryoglobulin associated GN general

A

Vasculitis associated with cold precipitable immunoglobulins

HCV common underlying infection

GN develops from precipitation of cryoglobulins in glomerular capillaries

165
Q

Cryoglobulin associated GN presentation

A

Purpuric and necrotizing skin lesions

Fever

Arthralgias

HSM

166
Q

Membranoproliferative GN

A

Nephritic along the entire spectrum, can also be nephrotic

Two types, type 1 more common

Immune complex deposition

167
Q

Membranoproliferative GN biopsy

A

Treat track appearance from double contours of GBM

Mesangial hypercellularity

168
Q

Difference in type 1 and type 2 membranoproliferative GN on electron microscopy

A

Type 1- subendothelial and eubepithelial deposits

Type 2- dense deposit disease, dense ribbons of C3 deposits

169
Q

Most common cause of nephrotic spectrum glomerular disease

A

Diabetes!

170
Q

Nephrotic spectrum general

A

Heavy proteinuria, >3 g/d

Edema, peripheral and generalized

Dyspnea

Hyperlipidemia

Hypoalbuminemia

171
Q

Minimal change disease general

A

Most common cause of proteinuric kidney disease in kids

Follows URI, tumor, etc.

172
Q

Minimal change disease presentation and diagnosis (biopsy)

A

Nephrotic syndrome

Diffuse obliteration of epithelial cell foot processes, but not specific for minimal change disease

173
Q

Membranous nephropathy (glomerulopathy) genearl

A

Most common cause of primary nephrotic syndrome in adults

50% progress to ESRD in 3-10 years

Immune mediated, accumulation of immune complexes in subepithelial zone

174
Q

Membranous nephropathy presentation

A

DVT is a common initial sign or renal vein thrombosis

175
Q

Renal biopsy for membranous nephropathy

A

Spike and dome pattern

176
Q

Focal segmental glomerulosclerosis general

A

Damage to podocytes

Chronic inciting issue

177
Q

FSGS biopsy

A

Sclerosis of some glomeruli

Fusions of epithelial foot processes

178
Q

Diabetic nephropathy general

A

Most common cause of ESRD in US

Initially increased GFR, then decreased when macro-albuminuria

179
Q

Renal amyloidosis general

A

Extracellular deposits of amyloid within the glomeruli (abnormally folded protein)

Secondary- from chronic inflammation

180
Q

Renal amyloidosis biopsy

A

Amyloid stains apple green with Congo red stain

Destruction of foot process

181
Q

HIV associated nephropathy

A

Collapsing pattern of focal sclerosis

Advanced HIV/AIDs patients

May have low CD4

182
Q

Simple renal cysts

A

Incidental finding on US or CT

Don’t lead to renal impairment

Periodic imaging, refer to urology

183
Q

Autosomal dominant polycystic kidney disease general facts

A

Often silent, half not diagnosed

50% develop ESRD by age 60

Genetic- systemic disease

184
Q

AD PKD pathology

A

Abnormal variants in proteins, affect structure of tissue

Leads to leakage and cyst formation

185
Q

AD PKD presentation

A 
Flank pain
Hematuria 
Proteinuria
Nephrolithiasis
HTN

Palpable kidneys on exam

186
Q

Complications of PKD

A 
Pain
Hematuria (recurrent bleeding in men >50 consider RCC)
Renal infection
Hypertension 
Cerebral aneurysm in circle of Willis
Heart disease
187
Q

Medullary sponge kidney general

A

Common and benign, autosomal dominant

Swiss cheese appearance from medullary cysts

188
Q

Medullary sponge kidney presentation

A

Hematuria
Neprhocalcinosis
Decreased urinary concentration

189
Q

Wilms tumor general

A

Most common malignant renal tumor of childhood

Painless abdominal mass id’d by parents

190
Q

What is the first line imaging for the kidney?

A

Ultrasound

191
Q

Renal cell carcinoma general

A

6th decade of life

Smoking contributes

192
Q

RCC presents with..

A

Hematuria
Flank pain
Abdominal mass

193
Q

Labs and imaging for RCC

A

increased EPO or anemia, hypercalcemia

Solid renal lesion is RCC until proven otherwise

CXR, may see cannonball mets

194
Q

What determines the stages for RCC?

A

Tumor size and degree of extension

195
Q

Main difference in I and II versus III and IV

A

3 and 4 have thickened walls, smooth or irregular with enhanced septa

Clin Med 2 (8 decks)

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