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
What kind of AKI is interstitial - caused by?
Drugs, infiltration with lymphoma, infection, tumour lysis syndrome following chemotherapy
26
What kind of AKI is vascular - caused by? what happens?
Vasculitis, malignant increased BP, thrombus or cholesterol emboli, large vessel dissection or thrombus.
27
Post renal AKI accounts for how much AKI and what is it caused by?
(10–25%) caused by urinary tract obstruction
28
Post Renal is caused by urinary tract obstruction what are the 3 types?
* Luminal—stones, clots, sloughed papillae * Mural—malignancy (eg ureteric, bladder, prostate) * Extrinsic compression—malignancy, retroperitoneal fibrosis
29
Risk factors for developing AKI? 9
* 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
30
Definition of chronic kidney disease?
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.
31
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?
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)
32
CKD?
Chronic kidney disease
33
When assessing a patient with known/suspected CKD try to identify possible cause which could be? what do you do?
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.
34
Stage 1 CKD: GFR? % of kidney function? Defined as?
Stage 1 of CKD has kidney damage with normal kidney function and GFR is 90 or higher with 90-100% of kidney function
35
Stage 2 CKD: GFR? % of kidney function? Defined as?
Kidney damage with mill loss of kidney function GFR is 89 to 60 and 89-60% of kidney function
36
Stage 3a CKD: GFR? % of kidney function? Defined as?
Mild to moderate loss of kidney function 59-45 = GFR 59-45% Function of kidney
37
Stage 3b CKD: GFR? % of kidney function? Defined as?
Moderate to severe loss of kidney function GFR 44-30 44-30% of kidney function
38
Stage 4 CKD: GFR? % of kidney function? Defined as?
Severe loss of kidney function GFR 29 to 15 29-15% of kidney function
39
Stage 5 CKD: GFR? % of kidney function? Defined as?
Kidney failure GFR less than 15% Less than 15%
40
CKD why is screening so important
Intervening early in CKD can reduce the progression to end-stage renal failure (ESRF)
41
Screening for CKD is recommended for at-risk patients with what? 8
* 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
What is renovascular hypertension?
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
Renovascular hypertension it is a renal response to reduced what?
Renal response to reduced renal perfusion = reduced perfusion of afferent arteriole
44
What happens to renin and RAAS with renovascular hypertension?
Renin release Activation of RAAS
45
There is increased BP with renovascular hypertension what happens directly and indirectly?
Directly -angiotensin II Indirectly – salt and water retention
46
SLIDE 14 - SEE diagrams What can be used to stop this RAAS activation associated with renovascular hypertension?
ACE inhibitors Ang II receptor blockers Stent
47
See slide 16 irreversible shock and renal failure
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
What is shock condition?
Critical condition caused by circulatory failure resulting in inadequate organ perfusion.
49
Shock renal condition is defined by?
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
Signs of shock?
Agitation, pallor, cool peripheries, tachycardia, slow capillary refill, tachypnoea, oliguria.
51
Shock can be due to inadequate cardiac output due to?
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
Hypovolaemia Bleeding? Fluid loss?
Bleeding: trauma, ruptured aortic aneurysm, GI bleed. Fluid loss: vomiting, burns, 'third space' losses (eg pancreatitis), heat exhaustion.
53
Pump failure due to?
Cardiogenic shock, eg ACS (heart muscle perfusion failure), arrhythmias, aortic dissection, acute valve failure.
54
Secondary causes of pump failure?
Secondary causes, eg pulmonary embolism, tension pneumothorax, cardiac tamponade
55
What is Glomerulonephritis? COVERED IN PREVIOUS LECTURES AS WELL
Inflammatory process primarily involving the glomerulus
56
Glomerular diseases can presents with?
Decreased GFR, proteinuria, hematuria, hypertension, oedema
57
How is the histological pattern of glomerular injury identified?
Renal biopsy
58
Obstruction in urinary tract has what effect?
Reduce urinary flow and impair renal function
59
When does glomerulonephritis usually occur?
More than one week after an infection
60
Glomerulonephritis usually occurs more than one week after an infection - referred to as?
Acute poststreptococcal glomerulonephritis
61
Common cause of glomerulonephritis comes from what infections?
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
What is Wegener vasculitis?
A progressive disease that leads to widespread inflammation of all of the organs
63
What systemic immune disease and then inflammatory disease of the arteries can cause glomerulonephritis?
Systemic immune disease such as systemic lupus erythematosus and Polyarteritis nodosa group - an inflammatory disease of the arteries.
64
Syndrome: Nephrotic 1. BP? 2. Urine? 3. GFR?
1. Normal to mild increase 2. Proteinuria > 3.5g/day 3. Normal to mild decrease
65
1. Common primary and 2. secondary causes of nephrotic syndrome?
1. Membranous, minimal change, FSGS, Mesangiocapillary GN 2. Diabetes, SLE (Class V nephritis), Amyloid, Hepatitis B/C
66
Nephritic syndrome 1. BP? 2. Urine? 3. GFR? 4. Primary causes? 5. Secondary causes?
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
A frequent effect of a partial or complete urinary tract obstruction is what?
A dilation of the renal pelvis (hydronephrosis)
68
Obstructions of the urinary tract are painful and need immediate treatment - why?
Due to the fail of renal function (reduced GFR)
69
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?
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
Slide 23 Obstructions of the urinary tract Where can they be and what can they be?
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
Calcium stones - what are the most common?
Calcium oxolate/calcium phosphate
72
Predisposing factors of calcium stones
Low urine volume and High urine calcium
73
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?
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
Calcium stones can be what in origin?
Idiopathic
75
Calcium stones can be associated with?
Increased intestinal calcium reabsorption, hypertension, obesity
76
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?
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
Control of micturition can be lost due to?
– a stroke – Alzheimer’s disease – CNS problems affecting cerebral cortex or hypothalamus
78
Sphincter muscles losing tone leads to?
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
In males urinary retention may develop due to?
If enlarged prostate gland compresses the urethra and restricts urine flow
80
SLIDE 29
81
Loss of bladder control - 2 types can be?
Neurogenic uninhibited bladder Atonic bladder
82
What happens in neurogenic uninhibited bladder?
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
What happens when an atonic bladder occurs?
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