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Gut, metabolism and hormones > Clinical scenarios - Renal 5 > Flashcards

Clinical scenarios - Renal 5 Flashcards

1
Q

Clinical scenarios
Consideration of physiology in context of these situations

A
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2
Q

Acidosis/alkalosis

A
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3
Q

During patient evaluation why might the presence of an acid-base disturbance be suspected?

A

The presence of an acid-base disturbance may be suspected on the basis of clinical presentation or by results of laboratory
data (e.g. a low HCO3-). Evaluation of any acid-base disorder can then be approached in a stepwise manner

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4
Q

In arterial blood normal acid-base parameters for pH, PaCO2, HCO3^-, PaO2?

A

pH = 7.35-7.45
PaCO2 = 35-45 mmHg
HCO3^- = 22-26 mEq/L
Normal PaO2 is 10.5–13.5kPa (75–100mmHg).

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5
Q

In arterial blood Acidosis acid-base parameters for pH, PaCO2, HCO3^- ?

A

pH < 7.35
PaCO2 > 45 mmHg
HCO3^- < 22 mEq/L

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6
Q

What is PaCO2?

A

Partial pressure of CO2 in arterial blood

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7
Q

In arterial blood Alkalosis acid-base parameters for pH, PaCO2, HCO3^-, PaO2?

A

pH > 7.45
PaCO2 < 35 mmHg
HCO3^- > 26 mEq/L

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8
Q

Bicarbonate reabsorption 80% is where?
6%? 4%?

A

~80% in PCT and ~10-15% in LoH:
* Mostly: Na+ /H+ antiporter [Na+/H+ exchanger 3 (NHE3)] - HCO3 − reabsorption via H+ secretion bNHE3.
* Some: Vacuolar H+ -ATPase - Apical H+ secretion for HCO3− reabsorption
~6% in DCT: Similar to above, some intercalated cells in late DCT
~4% in CT: Intercalated cells
(Note – % Values are approximate!)

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9
Q

PROBLEM:
A patient is found to have an arterial pH (pH = -log[H₃O⁺]) of 7.25, a plasma [HCO3-] of 14mM and a pCO2 of 33 mmHg.
What acid-base disturbance is present?

A

PaCO2 <4.5kPa (<35mmHg) indicates hyperventilation

A PaCO2 >6.0kPa (>45mmHg) indicates hypoventilation.
Bicarbonate (HCO3-): 22 to 26 milliequivalents per liter (mEq/L)

Acidosis, increased ventilation, metabolic acidosis, compensated by increased ventilation
=> Respiratory compensated metabolic acidosis

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10
Q

PaCO2 <4.5kPa (<35mmHg) indicates

A

Hyperventilation

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11
Q

PaCO2 <4.5kPa (<35mmHg) indicates

A

Hypoventilation

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12
Q

Early stages of respiratory compensated metabolic acidosis breathing is?
More severely it is?

A

Early stages: breathing is first rapid and shallow
More severe: Deep, labored gasping (Kussmaul breathing)

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13
Q

Acute renal failure what happens to GFR?

A

Acute fall in GFR - substances that are usually excreted by the kidney accumulate in the blood

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14
Q

Is acute renal failure fatal?

A

It can be fatal but it is often treatable

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15
Q

When is chronic renal failure usually diagnosed?

A

Not usually until 75% of function is lost

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16
Q

What kind of stage are you in when you have chronic renal failure?

A

Gradual and irreversible deterioration

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17
Q

Causes of acute renal failure the 3 stages?

A

Prerenal
Intrarenal
Postrenal

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18
Q

Explain the 3 causes of acute renal failure:
1. Prerenal
2. Intrarenal
3. Postrenal

A
  1. Sudden and severe drop in blood pressure (shock) or interruption of blood flow to the kidneys from severe injury or illness.
  2. Direct damage to the kidneys by inflammation, toxins, drugs, infection or reduced blood supply
  3. Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor or injury
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19
Q

AKI?

A

Acute kidney injury

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20
Q

Causes of AK?

A

Most common are ischaemia, sepsis and
nephrotoxins, prostatic disease causes up to 25% in some studies

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21
Q

Explain pre renal AKI:

A

(40–70%) due to renal hypoperfusion, eg
hypotension (any cause, including hypovolaemia, sepsis), renal artery stenosis

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22
Q

Explain intrinsic renal AKI: accounts for how much and what may it require?

A

10–50%) may require a renal biopsy for
diagnosis

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23
Q

Intrinsic renal AKI may be tubular explain:
1. What is the most common?
2. As a result of?
3.

A
  1. Acute tubular necrosis is the most common
    renal cause of AKI
  2. Often a result of pre-renal damage or
    nephrotoxins such as drugs (aminoglycoside antibiotics), crystal damage (eg ethylene glycol poisoning, uric acid), myeloma (abnormal light chain Ig).
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24
Q

What kind of AKI is glomerular? Caused by?

A

Autoimmune such as systemic lupus erythematosus, IgA vasculitis, drugs, infections (see lecture 1)

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25
Q

What kind of AKI is interstitial - caused by?

A

Drugs, infiltration with lymphoma, infection, tumour lysis syndrome following chemotherapy

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26
Q

What kind of AKI is vascular - caused by? what happens?

A

Vasculitis, malignant increased BP, thrombus
or cholesterol emboli, large vessel dissection or thrombus.

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27
Q

Post renal AKI accounts for how much AKI and what is it caused by?

A

(10–25%) caused by urinary tract obstruction

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28
Q

Post Renal is caused by urinary tract obstruction what are the 3 types?

A
  • Luminal—stones, clots, sloughed papillae
  • Mural—malignancy (eg ureteric, bladder, prostate)
  • Extrinsic compression—malignancy, retroperitoneal fibrosis
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29
Q

Risk factors for developing AKI? 9

A
  • Age >75
  • Chronic kidney disease
  • Cardiac failure
  • Peripheral vascular disease
  • Chronic liver disease
  • Diabetes
  • Drugs (esp newly started)
  • Sepsis
  • Poor fluid intake/increased losses
  • History of urinary symptoms
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30
Q

Definition of chronic kidney disease?

A

Impaired renal function for >3 months
based on abnormal structure or function, or GFR <60mL/min/1.73m2 (adult body surface area) for >3 months with or without evidence of kidney damage.

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31
Q

Classification of CKD -
1. How many stages?
2. Symptoms are recognised when?
3. End-stage renal failure is defined by?
4. Need for what treatment?

A
  1. 5 stages.
  2. Symptoms often only recognised once stage 4 is reached (GFR <30).
  3. End-stage renal failure (ESRF) is defined as GFR <15 mL/min/1.73m2
  4. Or need for renal replacement therapy (RRT—dialysis or transplant)
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32
Q

CKD?

A

Chronic kidney disease

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33
Q

When assessing a patient with known/suspected CKD try to identify possible cause which could be? what do you do?

A

Previous UTIS, LUTS (lower urinary tract symptoms), high BP, diabetes mellitus, systemic disorder, renal colic.
Check drug history and family history.
Systems review: always be on the lookout for
more than is immediately obvious, possible rare causes, symptoms suggestive of systemic
disorder or malignancy.

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34
Q

Stage 1 CKD: GFR? % of kidney function? Defined as?

A

Stage 1 of CKD has kidney damage with normal kidney function and GFR is 90 or higher with 90-100% of kidney function

35
Q

Stage 2 CKD: GFR? % of kidney function? Defined as?

A

Kidney damage with mill loss of kidney function GFR is 89 to 60 and 89-60% of kidney function

36
Q

Stage 3a CKD: GFR? % of kidney function? Defined as?

A

Mild to moderate loss of kidney function
59-45 = GFR
59-45% Function of kidney

37
Q

Stage 3b CKD: GFR? % of kidney function? Defined as?

A

Moderate to severe loss of kidney function
GFR 44-30
44-30% of kidney function

38
Q

Stage 4 CKD: GFR? % of kidney function? Defined as?

A

Severe loss of kidney function
GFR 29 to 15
29-15% of kidney function

39
Q

Stage 5 CKD: GFR? % of kidney function? Defined as?

A

Kidney failure
GFR less than 15%
Less than 15%

40
Q

CKD why is screening so important

A

Intervening early in CKD can reduce the progression to end-stage renal failure (ESRF)

41
Q

Screening for CKD is recommended for at-risk patients with what? 8

A
  • Diabetes mellitus
  • Hypertension
  • Cardiovascular disease (IHD, peripheral vascular disease, cerebrovascular disease)
  • Structural renal disease, known stones
  • Recurrent UTIs or those with childhood history of vesicoureteric reflux
  • Multisystem disorders which could involve the kidney, eg SLE
  • Family history of ESRF or known hereditary disease
  • Opportunistic detection of haematuria or proteinuria
42
Q

What is renovascular hypertension?

A

High blood pressure is caused by the kidneys’ hormonal response (renin release) to impaired blood supply to kidneys (for example due to narrowing of the arteries supplying the kidneys).

43
Q

Renovascular hypertension it is a renal response to reduced what?

A

Renal response to reduced renal perfusion =
reduced perfusion of afferent arteriole

44
Q

What happens to renin and RAAS with renovascular hypertension?

A

Renin release
Activation of RAAS

45
Q

There is increased BP with renovascular hypertension what happens directly and indirectly?

A

Directly -angiotensin II
Indirectly – salt and water retention

46
Q

SLIDE 14 - SEE diagrams
What can be used to stop this RAAS activation associated with renovascular hypertension?

A

ACE inhibitors
Ang II receptor blockers
Stent

47
Q

See slide 16 irreversible shock and renal failure

A

If there is a massive loss of fluids for example blood loss due to hameorrhage this will lead to reduced hypovolemia and reduced CO and person will go into shock and 1 effect of this is lack of perfusion to renal system - thus renal failure

Downstream effect of this in terms of symptoms is Oliguria which is reduced output of urine

48
Q

What is shock condition?

A

Critical condition caused by circulatory failure resulting in inadequate organ perfusion.

49
Q

Shock renal condition is defined by?

A

Often defined by low BP—(SBP) systolic <90mmHg—or mean arterial pressure (MAP)
<65mmHg— with evidence of tissue hypoperfusion, eg mottled skin, urine output
(UO) of <0.5mL/kg for 1 hour, serum lactate >2mmol/L.

50
Q

Signs of shock?

A

Agitation, pallor, cool peripheries, tachycardia, slow capillary refill, tachypnoea, oliguria.

51
Q

Shock can be due to inadequate cardiac output due to?

A
  1. Hypovolaemia - substainable in volume of blood in ECF cvould be caused by bleeding or trauma, aneurysm GI bleed, or fluid loss from heat exhaustion, third space losses, vomiting and burns
  2. Pump failure - heart stops working so cardiac function fails, cardiogenic shock, arrhythmias, aortic dissection and acute valve failure, it can also be a secondary event due to other reasons
52
Q

Hypovolaemia
Bleeding?
Fluid loss?

A

Bleeding: trauma, ruptured aortic aneurysm, GI bleed.
Fluid loss: vomiting, burns, ‘third space’ losses (eg pancreatitis), heat exhaustion.

53
Q

Pump failure due to?

A

Cardiogenic shock, eg ACS (heart muscle perfusion failure), arrhythmias, aortic dissection, acute valve failure.

54
Q

Secondary causes of pump failure?

A

Secondary causes, eg pulmonary embolism, tension pneumothorax, cardiac tamponade

55
Q

What is Glomerulonephritis? COVERED IN PREVIOUS LECTURES AS WELL

A

Inflammatory process primarily involving the
glomerulus

56
Q

Glomerular diseases can presents with?

A

Decreased GFR, proteinuria, hematuria, hypertension, oedema

57
Q

How is the histological pattern of glomerular injury identified?

A

Renal biopsy

58
Q

Obstruction in urinary tract has what effect?

A

Reduce urinary flow and impair renal function

59
Q

When does glomerulonephritis usually occur?

A

More than one week after an infection

60
Q

Glomerulonephritis usually occurs more than
one week after an infection - referred to as?

A

Acute poststreptococcal glomerulonephritis

61
Q

Common cause of glomerulonephritis comes from what infections?

A

A common cause of glomerulonephritis is from
a streptococcal infection, such as strep throat
or upper respiratory infection.

Typically seen in children from aged 3-12 years old not commonly seen in children yoinger

62
Q

What is Wegener vasculitis?

A

A progressive disease that leads to widespread inflammation of all of the organs

63
Q

What systemic immune disease and then inflammatory disease of the arteries can cause glomerulonephritis?

A

Systemic immune disease such as systemic
lupus erythematosus and Polyarteritis nodosa
group - an inflammatory disease of the
arteries.

64
Q

Syndrome: Nephrotic
1. BP?
2. Urine?
3. GFR?

A
  1. Normal to mild increase
  2. Proteinuria > 3.5g/day
  3. Normal to mild decrease
65
Q
  1. Common primary and 2. secondary causes of nephrotic syndrome?
A
  1. Membranous, minimal change, FSGS, Mesangiocapillary GN
  2. Diabetes, SLE (Class V nephritis), Amyloid, Hepatitis B/C
66
Q

Nephritic syndrome
1. BP?
2. Urine?
3. GFR?
4. Primary causes?
5. Secondary causes?

A
  1. Moderate to severe increase
  2. Haematuria (mild-macro)
  3. Moderate to severe decrease
  4. IGA nephropathy, mesangiocapillary GN
  5. Post streptoccal, vasculitis, SLE (other classes of nephritis), Anti-GBM disease, cryoglobulinaemia
67
Q

A frequent effect of a partial or complete urinary tract obstruction is what?

A

A dilation of the renal pelvis (hydronephrosis)

68
Q

Obstructions of the urinary tract are painful and need immediate treatment - why?

A

Due to the fail of renal function (reduced GFR)

69
Q

Slide 22
Pressures drive and oppose filtration of glomerulus
If there’s an increase in hydrostatic pressure in the the tubular component of the nephron in bowman’s capsule WHAT HAPPENS?

A

If there’s an increase in hydrostatic pressure in the the tubular component of the nephron in bowman’s capsule that will drive up the pressure which will counteract the glomerular capillary blood pressure causing a drop in Glomerular filtration rate (GFR)

70
Q

Slide 23
Obstructions of the urinary tract
Where can they be and what can they be?

A

Calculi and kidney stones can be formed in the cayx of the kidney in the pelvis of the kidney or in the ureters
Congenital pelviureteric junction obstruction
Fibrosis, tumours, haemorrhage which impair flow of urine to bladder
Cancer of surrounding organs such as in reproductive system: ovary, cervix, uterus, cancer of the bladder
Prostatic hypertrophy or cancer can all cause obstructions

71
Q

Calcium stones - what are the most common?

A

Calcium oxolate/calcium phosphate

72
Q

Predisposing factors of calcium stones

A

Low urine volume and High urine calcium

73
Q

Treatment of obstructions?
1. Stones less than 1cm?
2. Large stones?
3. What does it depend on?
4. What is lithotripsy?
5. Other 2 mechanisms to remove?

A

Relief of obstruction
1. Stones with diameters less than 1 cm may pass spontaneous
2. Larger stones require intervention
3. Depending on size, position, shape and composition
4. Lithotripsy (fragmentation of the stone i.e. ultrasonic)
5. Endoluminal extraction (endoscopic) and open surgical removal

74
Q

Calcium stones can be what in origin?

A

Idiopathic

75
Q

Calcium stones can be associated with?

A

Increased intestinal calcium reabsorption, hypertension, obesity

76
Q

Loss of urnairy bladder control why?
SLIDE 27 SEE DIAGRAM
*Also see renal lecture 2 for micturition pathway
1. PS: S24 does what?
2. Symp L2?
3. Somatic: motor pudental?

A

If any nerves in pathway are damaged it causes loss of function
1. Activates detrusor and inhibits internal sphincter
2. Inhibits detrusor and contracts internal sphincter
3. Activates external sphincter

77
Q

Control of micturition can be lost due to?

A

– a stroke
– Alzheimer’s disease
– CNS problems affecting cerebral cortex or
hypothalamus

78
Q

Sphincter muscles losing tone leads to?

A

Incontinence
When the muscles in and around the bladder don’t work the way they should, urine can leak, resulting in urinary incontinence. Incontinence can happen for many reasons, including urinary tract infections, vaginal infection or irritation, or constipation

79
Q

In males urinary retention may develop due to?

A

If enlarged prostate gland compresses the urethra and restricts urine flow

80
Q

SLIDE 29

A
81
Q

Loss of bladder control - 2 types can be?

A

Neurogenic uninhibited bladder
Atonic bladder

82
Q

What happens in neurogenic uninhibited bladder?

A

Partial crush of spinal cord may damage fibres that inhibit micturition reflex facilitation of reflex small volume of urine frequently voided in uncontrolled manner

83
Q

What happens when an atonic bladder occurs?

A

Compression of dorsal roots in sacral region
Loss of afferent fibers
Info from stretch receptors in bladder wall impaired
Normal tone of detrusor muscle lost
Micturition reflex abolished, although efferent fibers are intact
Bladder does not contract
Fills to capacity and urine lost through constant dribble from urethra

Gut, metabolism and hormones (22 decks)

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