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CPRII- Renal Exam > Path-1 > Flashcards

Path-1 Flashcards

1
Q

MCC of CRF (chronic renal failure)/ ESRD (end stage renal dz). Other causes?

A

DM

Other causes include autoimmune dz (IgA nephropathy; lupus)

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2
Q

Average kidney size?

A

Weight: 120-150 g
Length: 10-12 cm
Width: 6 cm
Thickness: 3 cm

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3
Q

Where does renal colic pain begin and where does it g?

A

Begins at renal angle )between lower 12th rib border and lateral border of Erector Spinae), travels down and forwards to groin.

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4
Q

Why is R kidney lower?

A

Because of the liver

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5
Q

What structures are anterior to the L kidney?

A 
Suprarenal gland
Spleen
Stomach
Pancreas
Left colic flexure
Jejunum
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6
Q

What structures are posterior to the L kidney?

A

Diaphragm
11th and 12th ribs
Psoas major, quadratus lumborum and transversus abdominis
Subcostal, iliohypogastric and ilioinguinal nerves

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7
Q

What structures are anterior to the R kidney?

A

Suprarenal gland
Liver
Duodenum
Right colic flexure

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8
Q

What structures are posterior to the R kidney?

A

Diaphragm
12th rib
Psoas major, quadratus lumborum and transversus abdominis
Subcostal, iliohypogastric and ilioinguinal nerves

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9
Q

How do surgeons divide the retroperitoneum to treat a retroperitoneal hemorrhage/neoplasm?

A

Into three zones!

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10
Q

Zone I

A

Called the central midline retroperitoneum.

Contains:

  • abdominal aorta
  • IVC
  • root of the mesentery
  • portions of the pancreas and duodenum
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11
Q

Zone II

A

Zone II is the lateral retroperitoneum

Contains:

  • kidneys
  • adrenal glands
  • renal vasculature
  • ascending and descending colon
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12
Q

Zone III

A

Called the pelvic retroperitoneum

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13
Q

Are the kidneys always paired?

A

NO

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14
Q

How do most kidney issues present?

A
  • Hematuria, proteinuria, oliguria, anuria
  • HTN
  • Edema
  • Labs: Increased serum/urine Cr, decreased Cr clearance, increased serum BUN
  • Can be asx
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15
Q

Most important Q to ask a pt suspected of having renal dz?

A

Have you ever had this before? B/c there is a big difference between acute and chronic kidney injury.

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16
Q

What is the “gatekeeper” of the cell?

A

Cell membrane becuase it provides cellular structure, protects cytosolic contents, and allows cells to be specialized. Phospholipid bilayer is responsible for keeping homeostasis.

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17
Q

Compartments of the kidney?

A

Glomeruli, tubules, interstitium, vessels

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18
Q

What compartment does DM primarily affect?

A

Glomeular (microvasculature)

But still could have tubulointerstitial features

19
Q

What compartment does systemic HTN primarily affect?

A

Vascular (arteriolar)…so this is a tubulointerstitial dz

20
Q

What is the general category of glomerular disorders due to?

A

Immunologic disorders…could be primary or secondary

21
Q

What causes the long term complications of DM?

A

Persistent hyperglycemia aka glucotoxicity

22
Q

What are the prototypes of the compartmental renal dz processes?

A
  • Glomeruli = glomerulonephritis
  • Tubules = Bence-Jones proteinuria
  • Interstitium = fibrosis, inflammation, or edema
  • Vessels = vasculitis, nephrosclerosis
23
Q

Azotemia

  • def
  • lab values
  • result of?
A
  • Biochemical abnormality
  • BUN and Cr elevation due to a decreased GFR
  • Result of renal disorders but could also come from extra-renal insults (pre-renal or post-renal)
24
Q

Prerenal azotemia

A
  • Happens after hypoperfusion of kidneys (hemorrhage, shock, volume depletion, CHF) –> leads to impaired renal fx
  • Impaired renal fx in absence of primary renal parenchymal damage
25
Q

Postrenal azotemia

A

-Obstruction! Distal to calyces and renal pelvis. Remove obstruction corrects the azotemia.

26
Q

Uremia definition

A

Azotemia + clinical sx resulting from renal damage

27
Q

What kind of sx does a uremia pt have?

A

Usually nonspecific. Get worse over time.

28
Q

Metabolic abnorms in uremia?

A

Anemia
Acidemia
Electrolyte abnormlaities

29
Q

How could a diabetic pt present if they have uremia?

A
  • May have better glycemic control as renal fx declines but they’ll have more hypoglycemic episodes.
  • This is paradoxical due to increased insulin secretion and prolongation of its t1/2
30
Q

What systems are affected (and their sx) in uremia?

A

Cardio: HTN, atherosclerosis, valvular stenosis, CHF, angina
GI: occult GI bleed; NV; uremic fetor breath
Neuro: fatigue, weakness, HA, amyloid deposits –> medial nerve neuropathy, carpal tunnel, or other nerve entrapments
Cutaneous: fluid retention, edema; calcium phosphate deposition and nail atrphy

31
Q

What do most uremic pt’s also present w/?

A

Peripheral neuropathy

32
Q

What are the general clinical signs of a pt w/ uremia?

A
  • NV, WL, faigue, anorexia
  • Pruritus
  • Polydipsia
  • Electrolyte issues –> muscle cramps
  • Encephalopathy
  • Bleeding –> due to platelet dysfx and anemia
  • Pericarditis
  • Pleuritis/ pleural diffusion
33
Q

Normal GFR?

A

90-120 mL/min/1.73 m^2

34
Q

Clinical sx of AKI

A
  • Rapid decline of GRF
  • Oliguria or anuria
  • Due to glomerular, interstitial, vascular, or acute tibular injury such as acute tubular necrosis
  • Reversible but can progress to CKD
35
Q

Clinical sx of CKD

A
  • Mild or silent
  • If severe –> uremia
  • Persistently decreased GFR (<60 mL/min for at least 3 months due to any cause)
  • Persistent albuminuria
  • Irreversible
36
Q

Clinical sx of ESRD

A

GFR <5% normal

End stage of uremia

37
Q

What are more characteristic of glomerular dz?

A
  • Nephritic and Nephrotic
  • Asx hematuira or proteinuria
  • Chronic Renal Failure
  • Acute Renal Failure
38
Q

What are more characteristic of tubulointerstitial dz?

A
  • UTI
  • Obstruction
  • Renal tumor
  • Nephrolithiasis
39
Q

Nephrotic Syndrome

A
  • Severe PROTEINURUA
  • Hypoalbuminemia
  • Severe edma
  • Hyperlipidemia
  • Lipiduria
40
Q

Nephritic Syndrome

A
  • Acute onset HEMATURIA
  • Mild–> mod. proteinuria
  • HTN
  • May also have edema but is less common
41
Q

Rapidly progressive glomerulonephritis

A

Nephritic syndrome signs + rapid decline in GFR

42
Q

What do you see w/ isolated urinary abnormalities?

A

Glomerular hematuria and/or subnephrotic proteinuria

43
Q

What could cause a glomerulus to be hypercellular?

A

Increased nuclei due to:

  1. Endothelial cells
  2. Mesangial cells
  3. VIsceral epithelia
  4. Inflammatory cell infiltrate
  5. Crescents (if you see this –> rapidly progressing glomerulonephritis)
44
Q

Histomorphologic features of glomerulopathies?

A
  • Hypercellularity
  • Basement membrane thickening and deposits
  • Hyalinosis (glassy)
  • Sclerosis (obliterative)
  • Issue w/ visceral epithelial cells could lead to an issue w/ the barrier

CPRII- Renal Exam (6 decks)

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