Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Stage 4 > Renal disease > Flashcards

Renal disease Flashcards

1
Q

Painful pins and needles + unable to distinguish hot and cold when bathing feet =

A

Wegener’s granulomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

First line renal Ix

A

USS

+ urinalysis for blood and protein (+urine microscopy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Red cell casts are diagnostic of what two conditions?

A

Glomerulonephritis

Vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 things cANCA means

A

It is associated with Wegener’s granulomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Microscopic vasculitis can cause?

A 
Episcleritis
Skin rashes
Joint pains
Nosebleeds
GI bleeding
Acute kidney injury
Chronic kidney disease
Pulmonary haemorrhage
Mono neuritis multiplex - pins and needles etc
Seizures due to intracerebral haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Crescents on renal biopsy indicates

A

Severe glomerular injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why act quick in rapidly progressive glomerulonephritis (RPGN)?

A

Patients can rapidly become unwell with multi-system symptoms
All c ANCA positive patients are at risk of developing pulmonary involvement
Rapid aggressive immunosuppression may salvage damaged nephrons and restore useful renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Duration of ABx in UTI
  2. Most common pathogen?
  3. Uncomplicated UTI first line Ix
  4. After recurrent UTIs what Ix?
  5. Non drug methods to reduce UTIs
  6. Prophylaxis for UTIs?
A
  1. 3 day
  2. E.coli then S. saprophyticus
  3. Urinalysis
  4. USS
  5. Pee after sex, Avoid barrier contraception, cranberry, increase fluids, probiotics
  6. Low dose, once daily ABx or single dose post sex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

CKD
Definition
Stages

A

Kidney damage OR GFR <60
For >3 months

1 = 60-89
2 = 45-59
3 = 30-44
4 = 15-29
5 = <15
5D = On dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

AKI criteria (2 ways and all within 1 week)

A

Serum creatinine rise of >26 over 48hrs OR rise of 1.5fold

Low urine output for over 6 hours

all occurred within 1 week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Indications for dialysis

A

Hyperkalemia

Acidosis

Fluid overload

Uraemic encephalopathy

Pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. First line Ix if suspected CKD/AKI to exclude obstruction
  2. Size of kindeys in CKD
  3. Asymmetry of renal tract =
  4. Unilateral enlargement of kidney
  5. diabetic drug CI in CKD
A
  1. USS
  2. Smaller
  3. Renal artery stenosis
  4. Hydronephrosis
  5. Metformin - lactic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. For nephrotic syndrome what must be known

2. How is proteinuria measured

A
  1. Low serum albumin. Proteinuria >3g/24hr. ACR or PCR

2. No longer 24hr collection. Now on the spot ACR or PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Biopsy in renal disease

A

Pre existing conditions such as DM mean that biopsy unneeded as likely to be DM nephropathy

Useful to detect glomerulonephritis (haematuria is a clue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Transferrin saturation is low thus meaning that acute blood loss is unlikely and cause is more liekly to be?

A

CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The most common explanation for anaemia in CKD is

A

Poor bioavailability of iron (uraemia reduces iron absorption aim for 20% saturation

EPO deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

EPO must be given in conjunction with?

A

Iron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What enzyme is affected in CKD which causes Vitamin D deficiency and then raised PTH to try and counteract the low calcium (secondary hyperparathyroidism - primary is where both are high)

A

1α hydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

why metabolic acidosis in CKD?

A

A metabolic acidosis is common in CKD due to reduced capacity to excrete the acid load generated during metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CKD is irreversible?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Reduce what from diet in CKD?

A

Phosphate and potassium and salt

22
Q

DM BP targets

A

130/80

normally <130/85

23
Q

Treat hyperphosphataemia in CKD

A

Yes - unpleasnt chalkty taste

24
Q 
CKD complication and management
Anaemia
Hyperkalemia
Hyperphosphotaemia
Sodium and fluid retention
Hyperparathyroidism
A

EPO + Iron

Restrict diet + dialysis if severe

Restrict diet + phosphate binders

Diuretics + antihypertensives

Vitamin D

25
Q

Absolute indications for dialysis

A

GFR <15
OR aeiou
A > Acidemia pH <7.1
E > electrolyte imbalance > hyperklaemia
I > Intoxication (drug or posion removal)
O > Oedema/overload (pulmonary oedema
U > Uraemia (encephalopathy and pericarditis

26
Q

CKD
Causes - District general hospital renal physician
Sx
Ix

A

Diabetes, Glomerulonephritis, Hypertension, Reflux, Polycystic kidneys

From stage 4 Loss of appetite, fatigue, sleepy, anuria, itching, HTN

Bloods: anaemia, low calcium, high phosphate, high ALP, high PTH

Urine: ACR/PCR, culture, dipstick

Imaging: USS - shrunken

Histology: If rapid or normal sized kidney and unclear cause

27
Q

Glomerulonephritis:
Eosinophils + RBC casts

Renal tubular casts + pigmented cells

RBCs + proteinuria >3g

A

Allergic interstitial nephritis

Acute tubular necrosis

Glomerulonephritis > Biopsy
Multiple myeloma > Serum and urine immunoelectrophoresis

28
Q

AKI
Prerenal - hyaline casts
Intrinsic
Postrenal

A

Transient hypoperfusion - hypotension, HF

Acute glomerulonephritis - inflammation of glomerular membrane
Allergic interstitial nephritis - allergic reaction to drugs
Acute tubular necrosis (>50%) - nephrotoxic agents causing prolonged renal hypoperfusion

Obstruction of urinary tract

29
Q

NSAIDS, ACEi and diuretics on prerenal AKI

A
  1. NSAIDs constrict afferent arterioole = Reduced GFR
  2. ACEi dilate efferent arteriole = reduced GFR … never give in RENAL ARTERY STENOSIS
  3. Diuretics reduce plasma volume and GFR
30
Q

Acute tubular necrosis - muddy brown!
Cause
Sx
Dx

A

AKI with renal cellular injury
Prolonged hypoperfusion, myeloma, drugs such as aminoglycosides, rhabdomyolysis

Oliguria ? polyuria > recovery

Urinary Na and FeNa are high as kidneys cannot reabsorb Na because tubules are damaged

Normal urinalysis

MUDDY BROWN CASTS
Coarsely granular casts

Biopsy: Abnormal tubular epithelium

31
Q

Allergic interstitial nephritis
Cause
Sx - TRIAD
Dx

A

Inflammation of the interstitium of the kidney causing AKI
Drugs - penicillin
Infection: Pyelonephritis

TRIAD: Myalgia, pyrexia and rash

Eosinophilia in urine and serum
Pyuria
White cell casts
NO BLOOD
Biopsy for definitive
32
Q

When are hyaline casts seen?

A

Prerenal

33
Q

High potassium =

A

ECG!

34
Q

A 65 year old women is admitted with back pain, fatigue and dehydration. Her Hb is 98, her Ur 18, her Cr is 250, adjusted Ca 3.1. What investigation will most help in the diagnosis?

A

Urine electrophoresis

35
Q

4 things when considering is this an AKI?

A

Monitor change in Cr – rise = AKI, maintained = CKD

Look for previous bloods to see Cr level– same = CKD

Ultrasound – Cortex is thin and kidney overall is shrunken = CKD

AKI if comes with NSAIDs or vomit/diarrhea

36
Q

CKD pathophysiology

A

Renal disease + proteinuria = loss of nephrons to fibrous tissue

These nephrons get poor perfusion and so blood is diverted to surviving glomerulus = increases filtration and pressure on remaining glomeruli = damages them further = vicious cycle

37
Q

Although ACEi are dangerous to AKi they are protective in CKD as they reduce ?

A

Proteinuria

38
Q

In CKD whats is gold standard treatment?

A

Transplant NOT haemodialysis

39
Q

Detailed CKD pathophysiology

A

Nephron number decreases in CKD so other nephrons increase their GFR to try and compensate (doesn’t work). So as hyperfiltration occurs more glomerular permeability occurs which lets through the filtration of more proteins, macromolecules and debris which = proteinuria > secondary dyslipidemia due to stimulation of liver synthesis across the board. AND nephrotoxic inflammation and remodeling due to the increased junk that filtered and cytokines such as TGF = fibrosis. ALSO RAAS is activated which causes hypertension. These combine to cause tubulointerstiail fibrosis and secondary Focal segmental glomerulo sclerosis which in turn causes anuria, low GFR and systemic complications such as uremia.

40
Q

Nephrotic syndrome

Definition and Sx

A

> 3.5g in 24h proteinuria

This level causes clinical hypoalbuminemia > decreased oncotic pressure > Oedema > liver produces more proteins to compensate some of which are lipoproteins which carry cholesterol = hyperlipidemia

Loss of anticoagulation factor = pro-thrombotic state = DVT, PE – anticoagulant once albumin is below 20

Lipoproteins from liver = increases cholesterol = rampant CVD

Loss of antibodies = increased risk of infection

41
Q

AKI definition

A

> 26.5 Cr rise in Cr within 48hours or low urine output.

There are 3 stages of Cr level/AKI severity

42
Q

AKI causes accumulation of which toxins

A

Urea: Pericarditis
Acidosis
Hyperkalemia: Tented T waves and wide QRS
Salt and water: Fluid overload

43
Q

How does quantity of proteinuria dictate cause

A

> 1g proteinuria = Significant = Glomeruloneprhitis and systemic diseases such as diabetes

<1g proteinuria = Modest = Tubulointerstitial disease, upper and lower UTI, kidney stones

44
Q

Post strep glomerulonephritis versus IgA nephropathy

A

Both come after URTI

PSGN presetns week after URTI, IgA is at the same time

PSGN shows immune complex and LOW complement + streptolysin O in blood

IgA nephropathy shows mesangial expansion with immune complexes

45
Q

Steps to quantifying proteinuria

A
  1. Urinalysis with dipstix
  2. Urine albumin/creatinine ratio >30
  3. 24 hour urine
46
Q

Proteinuria algorithm

A
  1. Assess BP
  2. Quantify proteinuria
  3. Assess GFR
  4. USS
  5. Special blood tests
  6. Biopsy
47
Q

ACEi and diabetic nephropathy

A

ACEi can help reduce proteinuria in CKD – dilatation of efferent arteriole HOWEVER don’t use in renal artery stenosis as they need to maximize GFR blood flow to kidney

48
Q 
Nephrotic syndrome
Minimal change disease
Presentation
Ix 
Biopsy
A

Children with atopy + hodgkins

Can’t see podocyte problem on light microscope NEED electron microscope

Responds well to steroids

49
Q 
Nephrotic syndrome
Focal Segmental Glomerulonephritis
Presentation
Ix
Biopsy
A

Young adult with HIV + FH

Antibodies test are negative

Segments of glomerular SCLEROSIS + IgM + Complement in basement membrane

50
Q 
Nephrotic syndrome
Membranous glomerulonephritis
Presentation
Ix
Biopsy
A

Older adults with malignancy

IgG deposits + thickened GBM

51
Q

Post renal
Cause
Sx
Ix

A

Stones or cancer

Nocturia, poor urinary flow, double micturition, oliguria, suprapubic mass

Raised Cr + large kidney on ultrasound

52
Q

Pre renal

A

Reduced renal perfusion

Low BP

Stage 4 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions