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Phase 4 Medicine > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

Define Nephrolithiais/Urolithiasis

A

Refers to the presence of crystalline stones (calculi) forming within the renal parenchyma or collecting duct, eventually moving to the urinary system (kidneys/ureter)

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2
Q

Give 5 main functions of the kidney (in normal health)

A

Fluid management

Red blood cell production (EPO production)

Acid Base Balance (Excretes H+ and reabsorbes HCO3-)

Waste excretion

Vitamin D metabolism (25-Hydroxyvitamin D to 1,25 Dihydroxyvitamin D)

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3
Q

Name 3 areas where ureteric stones tend to manifest?

A

Pelviureteric junction

Pelvic brim

Vesicoureteric junction

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4
Q

What can ureteric stones be comprised of? (2)

A

Calcium oxalate (most common)

Calcium phosphate (uncommon)

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5
Q

Give 4 risk factors for ureteric stone formation?

A

Male

Diet (excessive oxalate, urate, sodium and animal protein)

Chronic dehydration

Obesity

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6
Q

Give 1 complication of ureteric stone formation

A

Obstruction of urinary flow and infection

Obstruction can decrease eGFR and perfusion to the kidneys, leading to irreversible kidney damage.

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7
Q

Give 5 clinical features of a renal colic

A

Rapid/Abrupt onset (awoken from sleep)

Pain from loin to groin (comes and goes in waves)

Often cannot lie still (differentiates from peritonitis)

Worse on fluid loading

Nausea/Vomiting/Haematuria

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8
Q

What is used to diagnose ureteric/renal colic? (non-pregnant)

A

Non-contrast CT KUB (kidney, ureter and bladder) within 24 hours of admission

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9
Q

What is used to diagnose ureteric/renal colic? (pregnant)

A

Ultrasound

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10
Q

What additional tests may be important to consider for a patient with ?ureteric/renal colic? (4)

A

Urine dipstick - To exclude UTI

Creatinine and electrolytes - To assess renal function

FBC/CRP - To look for associated infection

Serum Calcium - To exclude cystinuria, uric acid stones and primary hyperparathyroidism

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11
Q

How is pain from ureteric/renal stones managed? (3)

A

1st line - IM Diclofenac
2nd line - IV Paracetamol
3rd line - Opioids

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12
Q

What medication is used to treat distal ureteric stones <10mm?

A

Tamsulosin (alpha blocker)

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13
Q

How do alpha blockers (like tamsulosin) treat renal stones?

A

Promote smooth muscle relaxation and dilation of the ureter, potentially easing stone passage

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14
Q

Describe the management of renal stones based on their size (4)

A

Watchful wait if <5mm and asymptomatic

5-10mm - shockwave lithotripsy

10-20mm - shockwave lithotripsy or ureteroscopy

> 20mm percutaneous nephrolithotomy

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15
Q

Describe the management of uretic stones? (2)

A

<10mm = Shockwave lithotripsy +/- alpha blockers

10-20mm ureteroscopy

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16
Q

Give 3 complications of shockwave lithotripsy

A

Shockwaves can cause solid organ injury

Fragmentation of larger stones can cause ureteric obstruction

Procedure may be uncomfortable and require analgesia afterwards

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17
Q

Give one indication for using ureteroscopy as opposed to lithotripsy to manage uretic stones

A

Pregnant female

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18
Q

Give 5 methods of preventing renal stones

A

High fluid intake

Add lemon juice to drinking water

Avoid carbonated drinks

Limit salt intake

Avoid thiazide diuretics

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19
Q

Define AKI. How is it characterised clinically?

A

Acute Kidney Injury

Describes an acute decline in kidney function (over hours/days), resulting in failure to maintain fluid, electrolyte and acid-base homeostasis.

Characterised by a rise in serum creatinine and/or a fall in urine output.

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20
Q

Give 3 divisions for causes of AKI

A

Pre-renal (most common)

Renal (intrinsic)

Post-renal (obstruction of urine outflow)

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21
Q

Give 5 risk factors for AKI

A

Sepsis

Major surgery

Cardiogenic shock (heart failure)

Hypovolemia

Drugs (ACEi, ARBs, NSAIDs, Iodinated contrast)

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22
Q

Give 4 drugs associated with causing AKI

A

ACEi (Ramipril)

ARBs (Candesartan)

NSAIDs (Ibuprofen)

Iodinated contrast

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23
Q

What electrolyte imbalances may be seen in AKI? (4)

A

Hyperkalaemia

Hyperphosphatemia

Hypermagnesemia

Hyponatraemia

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24
Q

Give 4 complications of AKI

A

Metabolic acidosis (altered consciousness, circulatory collapse, hyperventilation)

Volume overload (tachypnoea, tachycardia, cyanosis, lung crepitations)

Uraemia (high levels of urea in the blood)

CKD and end-stage renal disease

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25
Q

Give 5 clinical features of AKI

A

Nausea/Vomiting/Diarrhoea/Evidence of dehydration

Confusion, fatigue, drowsiness

Reduced urine output/changes in colour

Pulmonary/peripheral oedema + basal crepitations

Arrythmias (due to hyperkalaemia)

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26
Q

What diagnostic test is most important in detecting AKI?

A

U&E

Sodium, Potassium (most valuable), Urea and Creatinine (elevated)

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27
Q

What criteria are used to detect AKI?

A

p(RIFLE)

AKIN

KDIGO

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28
Q

Describe the KDIGO criteria for detecting AKI

A

Rise in serum creatinine of >26mmol/L within 48 hours.

A >50% rise in serum creatinine known or presumed to have occurred within the last 7 days

A fall in urine output to <0.5ml/Kg/hour for >6 hours in adults or >8 hours in children

A >25% fall in eGFR in children or young people within the last 7 days

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29
Q

Give 3 investigations which are important to conduct in a patient with ?AKI

A

Urinalysis (urine dipstick) - If shows haematuria and proteinuria without UTI/trauma, consider acute nephritis

Ultrasound - Gives assessment of kidney size

ECG - May show signs of hyperkalaemia

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30
Q

Give 4 signs of hyperkalaemia seen on an ECG

A

Flat/broad P waves

Tall tented T waves

Prolonged QRS

Prolonged PR

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31
Q

Describe how AKIs are staged according to KDIGO

A

Stage 1 = Creatinine = >26.5mmol/L and Urine Output = <0.5ml/Kg/h for 6-12h

Stage 2 = Creatinine = 2.0-2.9x baseline and Urine Output = <0.5ml/Kg/h for >12h

Stage 3 = Creatinine = >3x increase or increase of >353.6mmol/L and Urine Output = <0.3ml/Kg/h for 24h or anuria for 12h

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32
Q

Define pre-renal AKI

A

Characterised by reduced kidney perfusion (blood flow) resulting in ischaemia.

Typically leads to a decrease in GFR.

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33
Q

Give 3 pre-renal causes of AKI

A

Hypovolemia (decreased vascular volume) (haemorrhage, burns, pancreatitis)

Reduced cardiac output (heart failure, cardiogenic shock, liver failure, MI, sepsis)

Renal vasoconstriction (ACEi, ARBs, NSAIDs, Loop diuretics)

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34
Q

Define renal AKI

A

Characterised by structural damage to the kidneys

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35
Q

Give 4 causes of renal AKI

A

Toxins and Drugs (antibiotics, contrast, chemotherapy)

Vascular pathology (vasculitis, thrombosis, haemolytic uraemic syndrome, TTP, dissection, DIC)

Glomerular pathology (glomerulonephritis)

Tubular pathology (acute tubular necrosis)

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36
Q

Define post-renal AKI

A

Characterised by an acute obstruction of the outflow of urine, resulting in increased intratubular pressure and decreased GFR

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37
Q

Give 1 cause of post-renal AKI

A

Obstruction (renal stones, renal tract malignancy, enlarged prostate, blocked catheter)

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38
Q

How is pre-renal AKI primarily managed?

A

Correct volume depletion and/or increase renal perfusion

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39
Q

What medications should not be used to increase urine output/kidney perfusion respectively in pre-renal AKI?

A

Loop diuretics

Low dose dopamine

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40
Q

When (and only when) should loop diuretics be considered in a patient with pre-renal AKI?

A

When patient is awaiting renal replacement therapy.
or
When renal function is recovering in a patient not awaiting renal replacement therapy

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41
Q

How should renal cause of AKI be managed?

A

Refer for biopsy and specialist treatment for intrinsic renal disease

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42
Q

How should post-renal AKI be managed?

A

Refer for catheter, nephrostomy or urological intervention (stenting)

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43
Q

Give 3 other general managements of AKI

A

STOP nephrotoxic drugs (ACEi, ARB, NSAIDs, Genamicin, Amphotericin)

Treat hyperkalaemia (IV insulin + Dextrose + Calcium gluconate + nebulised salbutamol)

Treat metabolic acidosis (Sodium bicarbonate)

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44
Q

When should AKI patients be referred for Renal Replacement Therapy? (dialysis or transplantation)(4)

A

Hyperkalaemia

Metabolic acidosis

Symptoms or complications of uraemia (pericarditis/encephalopathy)

Fluid overload (peripheral/pulmonary oedema/crackles or basal crepitations)

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45
Q

Define CKD

A

Describes a reduction in kidney function and/or structural damage present for >3 months, with associated health implications.

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46
Q

What does GFR indicate?

A

Glomerular Filtration Rate

Describes how quickly blood is travelling through the kidney and so provides an indication to kidney function

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47
Q

What is the GFR of a normal functioning kidney?

A

> 60ml/min/1.73m2

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48
Q

Describe the 6 stages of CDK

A

Stage 1 (G1) = GFR = >90
(Only CKD if there is evidence of kidney damage, such as; Proteinuria and/or haematuria)

Stage 2 (G2) = GFR = 60-89 (Pathology on biopsy, tubular disorder, transplant)

Stage 3a (G3a) = GFR = 45-59 (Mild-moderate reduction in GFR)

Stage 3b (G3b) = GFR = 30-44 (Moderate-severe reduction in GFR)

Stage 4 = GFR = 15-29 (Severe reduction in GFR)

Stage 5 = GFR = <15 (Kidney Failure)

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49
Q

What are the 3 most common causes of CKD in the UK?

A

Diabetes (24%)

Glomerulonephritis (post-streptococcal -13%)

Hypertension (11%)

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50
Q

Give 8 complications of CKD (CRF HEALS)

A

C - Cardiovascular Disease
R - Renal osteodystrophy (decreased Ca, increased P04, increased pTH)
F - Fluid (oedema)

H - Hypertension
E - Electrolyte disturbances (K,H)
A - Anaemia (normocytic, normochromic due to reduced EPO production)
L - Leg restlessness
S - Sensory neuropathy

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51
Q

Give 6 clinical features of CKD

A

Fatigue

Oedema

Nausea +/- vomiting

Pruritis (due to urea accumulation from impaired renal excretion)

Restless legs (symptoms of uraemia)

Anorexia

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52
Q

Give 5 diagnostic tests used to investigate CKD

A

Renal ultrasound

Urine dipstick (test of haematuria)

Creatinine based eGFR

Albumin:Creatinine Ratio (test for proteinuria)

Biochemistry (may show raised PTH, Low Ca, High PO4 - vitamin D deficiency)

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53
Q

Describe the pharmaceutical management of CKD (2)

A

Blood pressure control - ACEi or ARB

Prevent/treat cardiovascular cause - Aspirin, Apixiban, Atorvastatin

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54
Q

Describe prostate cancer

A

Describes an adenocarcinoma arising from the peripheral zone of the prostate gland

Majority are multifocal

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55
Q

Prostate cancer is the most common cancer that metastasizes to what?

A

Bone

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56
Q

What is PSA?

A

Prostate Specific Antigen

Describes a protein produced by normal and cancerous prostate cells (isn’t prostate cancer specific).

Is secreted by the prostate epithelial cells into the prostatic fluid where it functions to liquify semen and allow spermatozoa to move more freely

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57
Q

Give 1 pro of using PSA

A

Early detection and early treatment

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58
Q

Give 4 cons of using PSA

A

False negative PSA tests - 15% of men with negative PSA may have prostate cancer

False positive PSA tests - 75% of men with a positive PSA test have a negative prostate biopsy

Unnecessary investigation - False positives may lead to invasive investigations (biopsy) which may have adverse effects (bleeding, infection ect)

Unnecessary treatment - Adverse effects from treatment, such as urinary incontinence and sexual dysfunction are common)

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59
Q

Give 6 risk factors for prostate cancer

A

Male

Increasing age

Black ethnicity

Family history - BRCA1, BRCA2, HOXB13

Overweight/obesity

Elevated testosterone

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60
Q

What is the main driver of prostate cancer formation?

A

Androgenic stimulation

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61
Q

What score is used to assess the likelihood that a patient has prostate cancer?

A

Likert score;

1 - Very unlikely
2 - Unlikely
3 - Difficult to tell
4 - Likely
5 - Very likely

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62
Q

What is the 1st line investigation for suspected prostate cancer? When is it’s use considered?

A

Multiparametric MRI

Offered if Likert scale is >=3

If Likert scale is 1-2 then discuss pros/cons of having a biopsy

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63
Q

What do NICE recommend with regards to PSA screening?

A

Men aged 50-69 should be referred if PSA is >=3.0ng/ml OR there is an abnormal DRE

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64
Q

Describe other investigations used in prostate cancer (3)

A

DRE - Examine size and structure of prostate

PSA - Determines risk (low, intermediate, high)

Prostate biopsy

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65
Q

Give 5 causes of raised PSA

A

Benign prostatic hyperplasia (BPH)

Prostatitis and UTI (NICE recommend postponing the PSA for 1 month after treatment)

Ejaculation

Vigorous exercise

Urinary retention

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66
Q

Give 5 clinical features of prostate cancer

A

Localised prostate cancer is often asymptomatic.

Bladder outlet obstruction (hesitancy, urinary retention)

Haematuria, haematospermia

Pain; back, perineal or testicular

DRE - Asymmetrical, hard, nodular enlargement with loss of medial sulcus

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67
Q

What may a digital rectal examination show in a patient with prostate cancer?

A

Asymmetrical, hard, nodular, enlargement with loss of medial sulcus

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68
Q

How is prostate cancer graded? Describe this

A

Graded using the Gleason Score.

Refers to how the cancer looks histologically on biopsy. The mor aggressive the cancer, the more malignant the cancer is.

Low risk = <6
Intermediate risk = 7
High risk = 8-10

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69
Q

How is prostate cancer staged? Describe this

A

Staged using TNM staging.

Refers to where the cancer is present in the body.

T1 – Clinically unapparent tumour (not detected by DRI nor visible through imaging)

T2 – Confined within the prostate
o T2a – Involves half a lobe or Less
o T2b – Involves > half of one lobe but not both
o T2c – Involves both lobes

T3 – Tumour extends through the prostate capsule but has not spread to other organs

T4 – Tumour is fixed or invades adjacent structures other than the seminal vesicles

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70
Q

How is localised prostate cancer managed?

A

Low/Intermediate risk;
- Active surveillance
- Radical prostatectomy
- Radical radiotherapy

High risk
- Offer either prostatectomy or radical radiotherapy
-Discuss option of Docetaxel Chemotherapy

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71
Q

Describe the active surveillance of low/intermediate risk prostate cancer (3)

A

Aim to keep patient with localised disease within a window of curability.

1st year - Involves testing PSA every 3-4 months and having a DRE after 12 months

2nd year - Involves testing PSA every 6 months and having DRE after 12 months

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72
Q

How is metastatic prostate cancer managed? (2)

A

External beam radiotherapy

Androgen deprivation therapy - Groserelin and Leuprorelin (LHRH antagonists)

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73
Q

Name 3 adverse effects of hormone therapy (treating prostate cancer) and describe how they are managed.

A

Hot flushes - Medroxyprogesterone

Sexual Dysfunction - Phosphodiesterase 5 inhibitors (sildenafil)

Osteoporosis - Bisphosphonates

74
Q

Define BPH

A

Benign Prostatic Hyperplasia

Describes enlargement of the inner (transitional) zones of the prostate.

Typically leads to lower urinary tract symptoms

75
Q

How may BPH present? (3)

A

Lower urinary tract symptoms;

Storage symptoms; Nocturia/Frequency/Urgency

Voiding symptoms; Poor stream/Hesitancy/Straining/Incomplete emptying/post void dribbling

Haematuria (may suggest cancer)

76
Q

Give 4 investigations used to assess BPH

A

Urinalysis - Investigate complicated UTI

DRE - prostate nodules/asymmetry more consistent with prostate cancer

PSA - Likely elevated

International Prostate Symptom Score - Used to classify the severity of LUTI symptoms to assess impact.

77
Q

How is BPH managed? (3)

A

Alpha blockers - Tamsulosin

5a reductase inhibitors - Dutasteride/Finisteride

Surgery - Transuretheral resection of prostate (TURP)

78
Q

Give 1 common side effect of Tamsulosin (alpha blocker)

A

Postural hypotension (alpha blockers induce dilation of venous capacitance vessels)

79
Q

In what patients is Dutasteride/Finasteride contraindicated?

A

5a reductase inhibitor

Contraindicated in patients with severe liver disease

80
Q

Give 1 possible complication of Transurethral resection of the prostate (TURP)

A

Impotency

81
Q

Give 4 possible side effects of 5 alpha reductase inhibitors (such as finasteride)?

A

Erectile dysfunction

Reduced libido

Ejaculation problems

Gynaecomastia

82
Q

What is the MOA of 5 alpha reductase inhibitors (such as finasteride)

A

Blocks conversion of testosterone to dihydrotestosterone (DHT), which is known to induce BPH

83
Q

How is a nephrotic syndrome characterised?

A

Characterised by proteinuria due to podocyte pathology

84
Q

What triad is seen in nephrotic syndrome?

A

Proteinuria (>3g/24h)

Hypoalbuminaemia (<30g/L)

Oedema

85
Q

How is nephritic syndrome characterised?

A

Characterised by haematuria due to inflammatory damage

86
Q

What symptoms are seen in nephritic syndromes? (4)

A

Haematuria + Red cast cells

Proteinuria > oedema

Hypertension

Oliguria and progressive renal impairment

87
Q

Name 3 nephrotic syndromes

A

Minimal change disease (most common - children)

Focal segmental glomerulosclerosis

Membranous nephropathy

88
Q

How does minimal change disease present in children? (4)

A

Triad; Proteinuria, Hypoalbuminaemia and Oedema

Facial/Leg oedema

Normotensive

No presence of haematuria

89
Q

How is minimal change disease diagnosed? What will it show?

A

Renal biopsy + Electron microscopy

Shows effacement (shortening) of podocyte foot processes

90
Q

How is minimal change disease treated? (2)

A

Relapse and remission

1st - Prednisolone
2nd - Cyclophosphamide

91
Q

Describe the prognosis of minimal change disease

A

1/3 have just one episode

1/3 have infrequent relapses

1/3 have frequent relapses which stop before adulthood

92
Q

Describe the proteinuria seen in minimal change disease

A

Only intermediate sized proteins (Albumin and transferrin) leak through the glomerulus

93
Q

Give 3 causes of minimal change disease

A

Drugs; NSAIDs/Rigampicin

Hodgkin’s lymphoma, thymoma

Infectious mononucleosis

94
Q

Describe focal segmental glomerulosclerosis

A

Describes a histological lesion characterised by segmental areas of glomerular sclerosis.

95
Q

Give 4 secondary causes of focal segmental glomerulosclerosis

A

HIV, Heroin, Lithium, Lymphoma

96
Q

Give 4 symptoms of focal segmental glomerulosclerosis

A

Triad of; Proteinuria, Hypoalbuminaemia and Oedema

Foamy Urine

Hypertension (Due to salt retention)

Xamthelasma/Xanthomata/Muehrcke’s lines (on nails)

97
Q

How is focal segmental glomerulosclerosis treated? (3)

A

1st - Prednisolone
2nd - Mycophenolate motefil + High dose dexamethasone

Adjunct- ACEi/ARB - to control blood pressure

98
Q

Describe membranous nephropathy

A

Most common nephrotic syndrome in adults.

Describes an immune mediated disease of the glomerular basement membrane.

99
Q

Give 4 causes of membranous nephropathy

A

Idiopathic - Due to anti-phospholipase A2 antibodies

Infection - Hep B, Malaria, Syphilis

Malignancy - Prostate, lung, lymphoma, leukaemia

Autoimmune disease - SLE, thyroiditis, rheumatoid

100
Q

What antibody may be present in idiopathic membranous nephropathy?

A

Anti-phospholipase A2 antibody (PLA2)

101
Q

What will a renal biopsy show in a patient with membranous nephropathy?

A

Thickened basement membrane with subepithelial electron dense deposits.

Creates a spike and dome appearance

102
Q

How is membranous nephropathy managed? (3)

A

ACEi/ARBs (reduces proteinuria)

Ponticelli regimen - Cyclophosphamide + Corticosteroid

Consider - Anticoagulation in high risk patients

103
Q

Name 5 types of nephritic syndrome

A

IgA nephropathy (most common)

Goodpastures (Anti-GBM)

Post-streptococcal

SLE

Haemolytic uraemic syndrome

104
Q

How is IgA nephropathy characterised on renal biopsy?

A

Characterised by mesangial deposition of IgA immune complexes

105
Q

Give 3 causes of IgA nephropathy

A

Alcoholic cirrhosis

Coeliac disease/dermatitis herptiformis

Henoch Schonlein purpura

106
Q

How does IgA nephropathy typically present?

A

Young male, presenting with recurrent episodes of macroscopic haematuria, typically following a respiratory tract infection.

107
Q

How does IgA Nephropathy differ from Post-Streptococcal glomerulonephritis? (3)

A

IgA - Develops 1/2 days after URTI
PSG - Develops 1-2 weeks after URTI

IgA - No Proteinuria
PSG - Proteinuria

IgA - Macroscopic haematoria
PSG - Low compliment

108
Q

How is IgA nephropathy managed?

A

No treatment if - Isolated haematorua, + no/minimal proteinuria (<500-1000mg/day) and normal eGFR

ACEi if - Persistent proteinuria (>500 - 1000mg/day) and reduced/normal eGFR

Corticosteroids if - Active disease (falling GFR or failure to respond to ACEi)

109
Q

Give 1 marker for a good prognosis in IgA nephropathy

A

Frank haematuria

110
Q

Give 4 markers for a poor prognosis in IgA nephropathy

A

Male gender

Proteinuria (>2g/day)

Hypertension

Hyperlipidaemia

111
Q

What triad is seen in haemolytic uraemic syndrome?

A

Microangiopathic haemolytic anaemia

Thrombocytopenia

AKI

112
Q

What majority of haemolytic uraemic syndrome cases in children are caused by what pathogen?

A

E.Coli (Shiga toxin producing)

113
Q

Describe goodpastures syndrome (Anti-glomerular basement membrane disease)

A

describes a small vessel vasculitis associated with pulmonary haemorrhage and progressive glomerulonephritis.

114
Q

Anti GBM antibodies are generated against what type of collagen? Where is this found?

A

Type IV collagen

Found in basement membranes of alveoli and glomeruli

115
Q

Give 3 features of goodpastures syndrome

A

Pulmonary haemorrhage > Haemoptysis

Rapidly progressive glomerulonephritis (Reduced urine output - AKI)

Oedema

116
Q

Describe the epidemiology of good pastures syndrome (2)

A

More common in males

Bimodal age distribution (peaks at 20-30 and then at 60-70)

117
Q

How is goodpastures diagnosed? What test confirms diagnosis?

A

Renal biopsy - Shows linear IgG deposits along basement membrane

Anti- GBM antibody titre - Confirms diagnosis

118
Q

How is goodpastures managed? (3)

A

Plasma exchange (plasmapheresis)

Oral Prednisolone

Cyclophosphamide

119
Q

What test is used to distinguish between AKI and CKD?

A

Renal Ultrasound

CKD patients have bilateral small kidneys

CKD patients also have hypocalcaemia (due to lack of vitamin D)

120
Q

What may be seen on histology in membranous glomerulonephritis? (3)

A

Basement membrane thickening on light microscopy

Subepithelial spikes on silver stain

Positive immunohistochemistry for PLA2

121
Q

Describe Primary Biliary Cholangitis. What is the classic presentation?

A

Describes an autoimmune condition where the immune system attacks the small bile ducts (intrahepatic) in the liver, resulting in obstructive jaundice and liver disease

Classic presentation = A middle aged woman presenting with itching

122
Q

Is primary biliary cholangitis intrahepatic or extrahepatic in nature?

A

Intrahepatic - Affects the small bile ducts within the liver

123
Q

Describe the pathophysiology of primary biliary cholangitis

A

Inflammation + damage to epithelial cells of bile ducts > Obstruction of bile flow through these ducts (cholestasis) > Liver fibrosis, cirrhosis and failure.

124
Q

Name 3 biochemical markers which may be raised in primary biliary cholangitis.

A

Bile acids

Bilirubin

Cholesterol

(All are usually excreted through the bile ducts into the intestine)

125
Q

Raised cholesterol increases the risk of what 2 diseases? And what 1 cosmetic symptom may it cause?

A

Increases risk of = Atherosclerosis and Cardiovascular Disease

Cosmetic symptom = Xanthelasma (cholesterol deposits in skin/tendons)

126
Q

Name 2 conditions associated with primary biliary cholangitis

A

Sjogren’s syndrome (seen in 80% of patients)

Rheumatoid arthritis

127
Q

Give 5 clinical features of primary biliary cholangitis

A

Pruritus (itching)

Jaundice

Pale, greasy stools

Dark urine

Xanthelasma/Xanthomata

128
Q

What 2 test results are positive in Primary Biliary Cholangitis? (2)

A

Autoantibodies = AMA (Anti-Mitochondrial Antibodies) - Most specific

Liver function tests = Raised ALP

129
Q

What is the most specific autoantibody marker for primary biliary cholangitis?

A

AMA (Anti-Mitochondrial Antibody)

130
Q

What other autoantibodies may be positive in primary biliary cholangitis?

A

Anti-nuclear antibody (35% of patients)

IgM (immunoglobulin M) (non specific)

131
Q

What imaging tools can be used to exclude extrahepatic biliary obstruction when investigating primary biliary cholangitis? (2)

A

Right Upper Quadrant Ultrasound

MRCP (magnetic resonance cholangiopancreatography)

132
Q

What is the 1st line treatment to slow disease progression and improve symptoms of primary biliary cholangitis?

A

Ursodeoxycholic acid

133
Q

What is the treatment for pruritus in primary biliary cholangitis?

A

Cholestyramine

134
Q

Give 3 complications of primary biliary cholangitis

A

Cirrhosis > Portal Hypertension > Ascites + Variceal haemorrhage

Osteomalacia and osteoporosis

Hyperlipidaemia (raised cholesterol)

135
Q

Define primary sclerosing cholangitis

A

Describes inflammation and damage to intrahepatic and extrahepatic bile ducts.

Results in sclerosis causing strictures that obstruct the flow of bile out of the liver into the intestines.

136
Q

Which form of IBD is strongly associated with primary sclerosing cholangitis?

A

Ulcerative colitis

137
Q

Give 4 clinical features of primary sclerosing cholangitis

A

Cholestasis = Jaundice, Pruritis, Raised bilirubin, Raised ALP

Right upper quadrant pain

Fatigue

Hepatomegaly/Splenomegaly

138
Q

What is the standard diagnostic investigation for primary sclerosing cholangitis? What will it show?

A

ECRP or MRCP

Shows multiple biliary strictures (beaded appearance)

139
Q

Which LFTs will be raised in primary sclerosing cholangitis?

A

Raised ALP

140
Q

Which autoantibodies may be positive in primary sclerosing cholangitis?

A

p-ANCA

ANA

Anti-Smooth Muscle Antibodies

141
Q

Name 2 complications/associations of primary sclerosing cholangitis

A

Ulcerative colitis

Cholangiocarcinoma

142
Q

What are gallstones predominantly made up of?

A

Cholesterol

143
Q

Name 3 possible complications of gallstones

A

Acute cholecystitis

Acute cholangitis

Pancreatitis (blocking the pancreatic duct)

144
Q

Which 2 ducts join to become the ampulla of Vater?

A

Common bile duct + Pancreatic Duct

145
Q

What is the name of the ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions into the duodenum?

A

Sphincter of Oddi

146
Q

Define cholecystitis

A

Inflammation of the gallbladder

147
Q

Define cholangitis

A

Inflammation of the bile ducts

148
Q

Define Biliary colic

A

Intermittent right upper quadrant pain caused by gallstones irritating the bile ducts

149
Q

Give 4 risk factors for gallstones (4Fs)

A

Fat
Fair
Female
Forty

150
Q

Give 4 symptoms of biliary colic

A

Right upper quadrant pain

Triggered by meals (high fat meals)

Pain lasts 30mins to 8 hours

Nausea and vomiting

151
Q

Why does ingestion of fat trigger biliary colic?

A

Fat causes cholecystokinin (CCK) secretion from duodenum > CCK triggers contraction of gallbladder > Biliary colic

152
Q

What is the 1st line investigation for gallstones?

A

Ultrasound

153
Q

What ultrasound findings may be present in a patient with gallstones? (3)

A

Gallstones in gallbladder/ducts

Bile duct dilatation (<6mm in diameter)

Acute cholecystitis (thickened gall bladder wall/fluid around gallbladder)

154
Q

If ultrasound is inconclusive, what imaging tool may be used?

A

MRCP

155
Q

What tool is used to clear stones from the bile ducts?

A

ERCP (Endoscopic retrograde cholangio-pancreatography)

156
Q

Give 4 complications of ERCP

A

Excessive bleeding

Duodenal perforation

Cholangitis

Pancreatitis

157
Q

What is the treatment for gallstones? (2)

A

Asymptomatic - Conservative management

Symptomatic - Laparoscopic cholecystectomy (removal of gallbladder)

158
Q

What is the imaging and treatment for acute cholecystitis?

A

Ultrasound and cholecystectomy

159
Q

Define ascending cholangitis

A

Bacterial infection (e.coli) of the biliary tree. Commonly caused by gallstones

160
Q

What bacteria most commonly causes ascending cholangitis?

A

E.coli

161
Q

What is Charcot’s triad? (Ascending cholangitis)

A

Right Upper Quadrant Pain

Fever

Jaundice

162
Q

What is the 1st line investigation for ascending cholangitis?

A

Ultrasound (look for bile duct dilatation and stones)

163
Q

How is ascending cholangitis managed? (3)

A

Fluid resuscitation

Broad spectrum IV antibiotics

ERCP after 24-48 hours

164
Q

Name 2 causes of acute pancreatitis

A

Alcohol excess

Gallstones

165
Q

Describe the pathophysiology of acute pancreatitis

A

Autodigestion of pancreatic tissue by pancreatic enzymes, leading to necrosis

166
Q

Give 4 features of acute pancreatitis

A

Severe epigastric pain (may radiate through back)

Vomiting

Epigastric tenderness, ileus and log-grade fever

Periumbilical discolouration (cullen’s sign) and flank discolouration (grey-Turner’s sign)

167
Q

Which 2 clinical signs may be present in acute pancreatitis

A

Cullen’s sign (Periumbilical discolouration)

Grey-Turner’s sign (Flank discolouration)

168
Q

Give 3 investigation for acute pancreatitis

A

Raised Serum Lipase (most specific and sensitive)

Raised Serum Amylase

Ultrasound

169
Q

When can a diagnosis of acute pancreatitis be made without an ultrasound scan?

A

If characteristic pain + Amylase/Lipase >3 times normal level

170
Q

What is the most sensitive and specific marker for acute pancreatitis?

A

Raised Serum Lipase

171
Q

What 3 scoring systems can be used to score acute pancreatitis?

A

Ranson score

Glasgow score

APACHE II

172
Q

Give 4 causes of acute pancreatitis

A

Gallstones and alcohol (Most common)

ERCP

Scorpion Venom

Drugs (azathiopurine, mesalazine, bendroflumethiazide)

173
Q

Give 3 complications of acute pancreatitis

A

Pseudocyts

Pancreatic necrosis

Pancreatic abscesses

174
Q

How is acute pancreatitis initially managed? (3)

A

Fluid resuscitation with crystalloids

Analgesia (IV opioids)

Enteral nutrition (if severe acute pancreatitis)

175
Q

How is acute pancreatitis managed surgically? (2)

A

Cholecystectomy (if due to gallstones)

ERCP (if due to obstructed biliary system)

176
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol excess

177
Q

Other than alcohol, give 3 causes of chronic pancreatitis

A

Cystic fibrosis

Haemochromatosis

Ductal obstruction (tumour, stones)

178
Q

Give 3 clinical features of chronic pancreatitis

A

Pain - Worse 15-30 minutes following a meal

Steatorrhea

Diabetes mellitus

179
Q

What investigations are used to diagnose chronic pancreatitis?

A

CT (shows pancreatic calcification) (most specific and sensitive)

Abdominal x-ray

Faecal elastase

180
Q

How is chronic pancreatitis managed? (4)

A

Abstinence from alcohol and smoking

Creon - Replacement of pancreatic enzymes

ERCP with stenting (if obstruction to biliary system/pancreatic duct)

Surgery (if pseudocysts, abscesses)

Phase 4 Medicine (15 decks)

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