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3a PTS - PM - ZTF > GP Conditions > Flashcards

GP Conditions Flashcards

1
Q

Type 2 Diabetes complications (3)

A

Infections e.g. candida
Macrovascular arterial e.g. coronary artery disease, stroke
Microvascular e.g. neuropathy, nephropathy, retinopathy

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2
Q

1st line medication to manage T2DM patients of any age with hypertension

A

ACE inhibitors

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3
Q

Medication started in T2DM when the patient has CKD with ACR above 30mg/mmol

A

SGLT-2 inhibitors

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4
Q

Type of medication used for erectile dysfunction

A

Phosphodiesterase-5 inhibitors e.g. sildenafil

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5
Q

4 options for neuropathic pain in diabetic neuropathy

A

Amitriptyline (TCA)
Duloxetine (SNRI)
Gabapentin (anticonvulsant)
Pregabalin (anticonvulsant)

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6
Q

Step-wise medical management of T2DM

A

1st line: Metformin, once settled ADD SGLT-2 inhibitor if the patient has CVD or HF or QRISK above 10%

2nd line: ADD sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor

3rd line: Triple therapy (metformin plus 2) or insulin therapy

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7
Q

Two side effects of SGLT-2 inhibitors

A

Increased frequency of UTIs and genital thrush more glucose in the wee due to inhibiting reabsorption
Diabetic ketoacidosis

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8
Q

T2DM diagnostic results (3)

A

HbA1c > 48
Fasting plasma glucose > 7
Random plasma glucose: > 11.1

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9
Q

Pre-diabetes HbA1c

A

42-47 mmol/mol

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10
Q

Pathophysiology of T1DM

A

Autoimmune disorder where the insulin producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system

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11
Q

Main side effects of insulin treatment

A

Hypoglycaemia
Weight gain
Lipodystrophy

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12
Q

MOA metformin (3)

A
  1. Increase insulin sensitivity
  2. Decreases hepatic gluconeogenesis
  3. Decreases intestinal absorption of glucose
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13
Q

Metformin side effects

A

GI upset
Lactic acidosis

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14
Q

Secondary hyperthyroidism definition

A

Pathology in the hypothalamus or pituitary producing too much TSH

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15
Q

Graves’ disease definition

A

Autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism

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16
Q

Most common cause of hyperthyroidism / thyrotoxicosis

A

Graves’ disease

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17
Q

Which condition causing hyperthyroidism is most common in patients over 50

A

Toxic multinodular goitre

nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones

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18
Q

Pathophysiology of exophthalmos (proptosis)

A

Bulging of the eyes caused by Graves’ disease

inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets

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19
Q

Pretibial myxoedema definition

A

Skin condition caused by glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area)

Gives the skin a discoloured, waxy, oedematous appearance over this area

Specific to Graves’ disease and is a reaction to TSH receptor antibodies

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20
Q

Causes of hyperthyroidism (4)

A

GIST:

Graves’ disease
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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21
Q

Thyroiditis (thyroid gland inflammation) disease pattern

A

Initial period of hyperthyroidism followed by hypothyroidism

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22
Q

4 causes of thyroiditis

A

De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis

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23
Q

Graves’ disease specific features

A

Diffuse goitre (w/o nodules)
Graves’ eye disease with exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)

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24
Q

Presentation of hyperthyroidism

A

Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination

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25
Q

1st line anti-thyroid drug

A

Carbimazole, usually taken for 12 to 18 months

Methods of dosing:
- Titrate to maintain normal levels
- Block all production and replace with levothyroxine

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26
Q

2 complications of carbimazole use

A

Acute pancreatitis (look for severe epigastric pain radiating to back)
Agranulocytosis (look for susceptible to infections/sore throat)

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27
Q

Blood results of thyrotoxicosis (e.g. Graves’)

A

TSH: low
Free T4: high

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28
Q

Antibodies found in Graves’ disease

A

TSH receptor antibodies

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29
Q

Antibodies found in Hashimoto’s thyroiditis

A

anti-TPO antibodies

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30
Q

1st line symptomatic management of hyperthyroidism

A

Propranolol

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31
Q

Most common cause of hypothyroidism in the developed world

A

Hashimoto’s thyroiditis

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32
Q

Most common cause of hypothyroidism in the developing world

A

Iodine deficiency

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33
Q

Presentation of hypothyroidism

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

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34
Q

Treatment of hypothyroidism

A

Oral levothyroxine (synthetic T4 which metabolises to T3)

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35
Q

Investigations following a hypertension diagnosis

A

Fundoscopy: to check for hypertensive retinopathy
U+Es, Urine dipstick: to check for renal disease (as a cause or consequence of)
ECG: left ventricular hypertrophy or IHD
HbA1c: check for co-existing DM (CVD RF)
Lipids: check for hyperlipidaemia (CVD RF)

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36
Q

Hypertension stage 1 definition

A

ABPM/HBPM monitoring = > 135 / 85 mmHg

Or

Clinic reading persistently = > 140 / 90 mmHg

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37
Q

Step 1 management for hypertension in patient who is <55 or T2DM

A

1st line: ACE inhibitor
2nd line (e.g. because of ACEi cough side effect): Angiotensin 2 Receptor blocker

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38
Q

Step 1 management for hypertension in patient who is >55 or Afro-Caribbean with NO T2DM

A

1st line: Calcium channel blocker

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39
Q

Step 2 management for hypertension

A

ACEi/A2RB + CCB

OR

ACEi/A2RB + thiazide-like Diuretic

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40
Q

Step 3 management for hypertension

A

ACEi/A2RB + CCB + thiazide-like D

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41
Q

Step 4 management of hypertension based on K+ results

A

K+ < 4.5 add low dose spironolactone

K+ > 4.5 add alpha or beta blocker

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42
Q

Stage 2 hypertension definition

A

Clinic BP > 160/100
ABPM/HBPM > 150/95

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43
Q

Severe hypertension definition

A

Clinic systolic > 180 mmHg
Clinic diastolic > 120 mmHg

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44
Q

What would indicate a same-day specialist review in BP 180/120 mmHg

A

Retinal haemorrhage or papilloedema
Life threatening symptoms (new onset confusion, chest pain, HF Sx, AKI)
Suspected phaeochromocytoma (labile or postural hypotension, headache)

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45
Q

Single most common cause of secondary hypertension

A

Primary hyperaldosteronism (Conn’s)

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46
Q

Renal conditions which would increase BP

A

Glomerulonephritis
Pyelonephritis
APKD
Renal artery stenosis

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47
Q

Drug causes of secondary hypertension

A

Steroids
MAOIs
COC
NSAIDs (by blocking prostaglandins)

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48
Q

Top differentials for a non blanching rash (bleeding under the skin)

A

Leukaemia
Meningococcal septicaemia
Henoch-schonlein purpura
ITP
TTP
Traumatic

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49
Q

Analgesia management in osteoarthritis

A

1st line: topical NSAIDs (particularly beneficial for OA of knee or hand)
2nd line: oral NSAIDs - a PPI should be co-prescribed e.g. omeprazole

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50
Q

Characteristic features of OA of the hand

A

Unsymmetrical

Carpometacarpal (CMC) and distal interphalangeal (DIP) joints

Heberden’s nodes at the DIP pints
Bouchard’s nodes at the PIP joints

Squaring of the thumbs (fixed adduction)

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51
Q

X-ray investigation results of OA

A

LOSS:
Loss of joint space
Osteophytes forming at joint margins
Subchondral sclerosis
Subchondral cysts

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52
Q

Diagnosis of OA w/o investigations

A

Over 45, typical pain associated with activity and has no morning stiffness (or stiffness lasting under 30 minutes)

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53
Q

Which patients is OA most commonly seen in

A

Post-menopausal women (due to loss of protective oestrogen)

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54
Q

Gout definition

A

A type of crystal athropathy associated with chronic hyperuricaemia

Urate crystals are deposited in the joint, causing it to become inflamed

Episodes last several days with symptom-free periods in between

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55
Q

Gout typical presentation

A

Single acute hot, swollen painful joint (key DDx: septic arthritis)
Gouty tophi (subcutaneous uric acid in the hands, elbows and ears)

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56
Q

Risk factors for gout

A

Male
FHx
Obesity
High purine diet (meat and seafood)
Alcohol
Diuretics
CVD
Renal disease

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57
Q

Most commonly affected joints in gout

A

Base of the big toe: metatarsophalangeal joint (MTP joint) - 70% of first presentations affect 1st MTP
Base of the thumb: carpometacarpal joint (CMC joint)
Wrist

Gout can also affect larger joints e.g. knee and ankle

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58
Q

Diagnosis of gout

A

Clinical diagnosis
- supported by a raised serum urate level on blood test (typically checked 2 weeks later as may be high, normal or low during acute attack)

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59
Q

Aspirated joint fluid 2 findings in gout that differentiate it from septic arthritis and pseudogout

A
  1. No bacterial growth (important to exclude septic arthritis)
  2. Monosodium urate crystals: needle shaped and negatively birefringent of polarised light (PseudOgOut = rhOmbOid shaped and Positively birefringent)
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60
Q

X-ray findings in gout

A

No loss of joint space
Lytic lesion in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanging edges

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61
Q

Management of acute flares of gout

A

1st line: NSAIDs e.g. naproxen - co-prescribed with PPI
2nd line: colchicine (if renal impairment or significant heart disease)
3rd line: oral steroids e.g. prednisolone

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62
Q

Gout prophylaxis

A

Xanthine oxidase inhibitors which lower uric acid level e.g. Allopurinol (1st) or Febuxostat (2nd)
- offered to all patients after their first attack of gout

  • Prophylaxis is not started until inflammation has settled after the acute attack (NSAIDs/colchicine can be continued)
  • Once established on allopurinol, continue during future acute attacks
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63
Q

Main side effect of colchicine

A

Diarrhoea

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64
Q

4 causes of acute liver failure

A

Paracetamol overdose
Alcohol
Viral hepatitis (usually A or B)
Acute fatty liver of pregnancy

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65
Q

Features of acute liver failure

A

Jaundice
Coagulopathy: raised PT time
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure is common (hepatorenal syndrome)

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66
Q

Differentiating features of Crohn’s disease

A

‘Crows’ NESTS:

N - No blood or mucus (PR bleeding is less common)
E - Entire GI tract (mouth to anus)
S - ‘Skip’ lesions on endoscopy
T - Terminal ileum most affects and Transmural inflammation
S - Smoking is a risk factor

+ strictures and fissures

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67
Q

Differentiating features of Ulcerative Colitis

A

You See (UC) CLOSE UP:

C - Continuous inflammation
L - Limited to the colon and rectum
O - Only superficial mucosa affected
S - Smoking may be protective (UC less common in smokers)
E - Excrete blood and mucus
U - Use Aminosalicylates
P - Primary sclerosing cholangitis

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68
Q

Blood tests for IBD investigations

A

FBC: Hb (anaemia), platelet count (raised w inflammation)
CRP
U&Es: electrolyte imbalance, kidney function
LFTs: low albumin in severe disease (protein lost in bowel)
TFTs: hyperthyroidism as DDx for diarrhoea
Anti-TTG: coeliac

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69
Q

IBD screening and diagnostic investigations

A

Screening: faecal calprotectin (90% sensitive and specific)
Diagnostic: colonoscopy with multiple intestinal biopsies

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70
Q

UC management

A

Mild to moderate:
1st line = Aminosalicylate e.g. mesalazine
2nd line = Corticosteroids e.g. oral/PR prednisolone

Acute severe:
1st line = IV steroids e.g. IV hydrocortisone

Maintaining remission: aminosalicylate, Azathioprine, mercaptopurine

Panproctocolectomy will remove the disase = patient will have ileostomy or J pouch

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71
Q

Crohn’s management

A

1st line in inducing remission: glucocorticoids e.g. oral pred or IV hydrocortisone

1st line in maintaining remission: Azathioprine, mercaptopurine

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72
Q

Most common cause of hyperthyroidism in pregnancy

A

Graves disease

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73
Q

Cushing’s disease

A

Cushing’s syndrome caused specifically by a pituitary gland tumour

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74
Q

Causes of Cushing’s syndrome

A

High/chronic doses of exogenous steroids (most common cause)
Pituitary gland tumour (Cushing’s disease) - most common endogenous/ACTH dependent cause
Adrenal tumour (excessive cortisol)
Paraneoplastic ectopic ACTH i.e. small cell carcinoma in the lungs

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75
Q

5 mechanisms of cortisol

A

Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness

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76
Q

electrolyte imbalance associated with ectopic ACTH secretion

A

Hypokalaemia

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77
Q

1st line / Gold standard test to diagnose Cushing’s syndrome

A

Overnight (low-dose) dexamethasone suppression test

high-dose test can be used to localise pathology e.g. cortisol + ACTH suppressed = pituitary adenoma)

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78
Q

Most common cause of primary hyperaldosteronism (Conn’s)

A

bilateral idiopathic adrenal hyperplasia

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79
Q

Features of primary hyperaldosteronism (Conn’s)

A

Hypertension
Hypokalaemia e.g. muscle weakness
Hypernatraemia
Metabolic alkalosis

aldosterone causes sodium retention and resulting potassium excretion in the kidneys

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80
Q

1st line investigation in Conn’s

A

Plasma aldosterone:renin ratio

= high aldosterone/low renin: aldosterone causes sodium retention which has a negative feedback on renin

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81
Q

Management of Conn’s (bilateral adrenocortical hyperplasia)

A

Aldosterone antagonist e.g. spironolactone

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82
Q

Renal colic definition

A

Unilateral loin to groin pain
Colicky (flucuating in severity)

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83
Q

Investigation renal colic

A

CT KUB (CT of the kidneys, ureters and bladder) within 24 hours of presentation

Ultrasound should be used for pregnant women and children

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84
Q

Presentation of hypercalcaemia/hyperparathyroidism

A

Renal stones
Painful bones
Abdominal groans
Psychiatric moans

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85
Q

3 causes of hypercalcaemia

A

Calcium supplementation
Hyperparathyroidism
Cancer (e.g. myeloma, breast, lung)

86
Q

Most common type of renal stone

A

Calcium oxalate

87
Q

Complications of renal stones (2)

A

Obstruction (leading to acute kidney injury)
Infection (obstructive pyelonephritis)

88
Q

Presentation of renal stones

A

Renal colic
Haematuria

89
Q

Most effective type of analgesia for renal stones

A

NSAIDs e.g. IM diclofenac

2nd line: IV paracetamol

90
Q

Renal stones <5mm management

A

Watchful waiting (50-80% will pass)

Tamsulosin (alpha blocker) can be used to help aid passing

Surgical intervention: stones >10mm, won’t pass, signs of infection

91
Q

Thiazide diuretic MOA in prevention of renal stones

A

Prevention of hypercalciuria by increasing distal tubular calcium resorption

92
Q

2 prerenal causes of AKI

A

Hypovolaemia (secondary to D+V)
Renal artery stenosis

both cause lack of blood flowing to the kidneys/ischaemia

93
Q

2 renal causes of AKI

A

glomerulonephritis
rhabdomyolysis

94
Q

2 postrenal causes of AKI

A

renal stones
benign prostatic hyperplasia

95
Q

Nephrotoxic drugs (5)

A

NSAIDs e.g. ibuprofen, aspirin can be continued at a cardioprotective 75mg dose
amingolycoside antibiotics e.g. gentamicin
ACE inhibitors e.g. ramipril
Angiotensin II receptor antagonists (ARBs) e.g. candesartan
Diuretics e.g. furosemide

96
Q

Stage 1 AKI

A

urine output of less than 0.5 ml/kg/hour for ≥ 6 hours
OR
Increase in creatinine to 1.5-1.9 times baseline

97
Q

Stage 2 AKI

A

urine output of less than 0.5 mL/kg/hour for ≥ 12 hours
OR
Increase in creatinine to 2.0 to 2.9 times baseline

98
Q

Stage 3 AKI

A

urine output of less than 0.3 mL/kg/hour for ≥24 hours
OR
Increase in creatinine to ≥ 3.0 times baseline

99
Q

Bladder cancer features (5)

A

frequency
urgency
nocturia
weight loss
painless haematuria

100
Q

1st line investigation bladder cancer

A

cystoscopy and biopsy

101
Q

2 major risk factors for transitional cell carcinoma of the bladder

A

Smoking
Exposure to aniline dyes

102
Q

H. pylori treatment

A

1 PPI + 2 antibiotics + lifestyle modifications

e.g. lansoprazole + clarithromycin + metronidazole + stop smoking/caffeine

103
Q

gastric ulcer vs duodenal ulcer pain

A

gastric ulcer = pain IMMEDIATELY after eating

104
Q

CKD stages

A

Stage 1: > 90 mL + abnormal kidney tests
Stage 2: 60-89 mL + abnormal kidney tests (-30)
Stage 3A: 45-59 mL (-15)
Stage 3B: 30-44 mL (-15)
Stage 4: 15-29 mL (-15)
Stage 5/ESRF: <15mL

105
Q

Ratio investigating proteinuria in CKD

A

albumin:creatinine ratio (ACR)

106
Q

Management of CKD patients where ACR >30

A

1st line: ACE inhibitors
other: SGLT-2 inhibitors

107
Q

How does CKD impact bone health

A

high phosphate (not being excreted in kidneys) drags calcium from the bones resulting in osteomalacia

secondary hyperparathyroidism (low calcium, low vitamin D, high phosphate)

108
Q

renal ultrasound differentiation of CKD and AKI

A

bilateral small kidneys in CKD

109
Q

how does CKD lead to anaemia

A

reduced erythropoietin levels

110
Q

COPD stepwise treatment pathway (steroid responsive)

i.e. asthmatic features/atopic illness/FEV1 variation

A

Step 1: SABA e.g. salbutamol or SAMA e.g. ipratropium bromide
Step 2: SABA + LABA + ICS e.g. beclomethasone (if they were originally on SAMA, discontinue and start SABA)
Step 3: SABA + triple therapy i.e. LABA + ICS + LAMA e.g. tiotropium

111
Q

COPD stepwise treatment pathway (non-steroid responsive)

i.e. no asthmatic features/no atopic illness/no FEV1 variation

A

Step 1: SABA or SAMA
Step 2: SABA + LABA + LAMA (if they were originally on SAMA, discontinue and start SABA)

112
Q

Drug classes in asthma/COPD treatment and examples

A

SABA = short acting beta 2 agonist e.g salbutamol
LABA = long-acting beta 2 agonist e.g salmeterol
SAMA = short-acting muscarinic antagonist e.g ipratropium
LAMA= long-acting muscarinic antagonist e.g tiotropium
ICS = inhaled corticosteroid e.g. beclometasone, fluticasone

113
Q

Moderate asthma definition

A

PEFR 50-75% best or predicted
Speech normal

114
Q

Severe asthma definition

A

PEFR 33 - 50% best or predicted
Can’t complete sentences

115
Q

Life threatening asthma definition + signs

A

PEFR < 33% best or predicted
Oxygen sats < 92%
‘Normal’ pC02 (4.6-6.0 kPa)
Silent chest, cyanosis or feeble respiratory effort
Bradycardia, dysrhythmia or hypotension
Exhaustion, confusion or coma

116
Q

Feature of ‘near-fatal asthma’

A

Raised pCO2 > 6 kPa

117
Q

Management for life threatening asthma

A

1st line Nebulised SABA (salbutamol) delivered in O2

Nebulised ipratropium bromide

Oral prednisolone for 5 days

118
Q

positive asthma reversibility test

A

Improvement in FEV1 of 12% or more after inhalation of SABA

119
Q

QRISK score

A

Risk of developing a heart attack or stroke in the next 10 years

>10% = benefit from a prescribed statin

120
Q

3 key investigations in MI

A

ECG
CXR
Cardiac enzymes (troponin, myoglobin and creatinine kinase)

121
Q

Primary hyperparathyroidism

A

Excess secretion of PTH resulting in hypercalcaemia

most common cause of hypercalcaemia in outpatients

122
Q

Cause of 85% of primary hyperparathyroidism

A

Solitary adenoma

123
Q

Primary hyperparathyroidism investigations

A

Bloods: high calcium, low phosphate
X-ray: pepperpot skull

124
Q

What has occurred when PTH still not corrected after correcting underlying cause of secondary hyperparathyroidism

A

Secondary has caused hyperplasia of parathyroid glands = tertiary

125
Q

2 main causes of secondary hyperparathyroidism

A
  1. Low vitamin D
  2. CKD

= cause low calcium which causes high PTH

126
Q

Acute bacterial endocarditis contraindicated medication

A

Heparin

127
Q

Rheumatoid arthritis hand signs (4)

A

Z-shaped deformity
Swan neck deformity
Boutonniere deformity
Ulnar deviation

128
Q

Causes of clubbing

A

Cardiac = atrial myxoma, cyanotic heart disease, endocarditis, pericarditis

Gastrointestinal = malabsorption, inflammatory bowel disease, liver cirrhosis

Respiratory = Cystic fibrosis, Tuberculosis, Pulmonary fibrosis, bronchiectasis, bronchial carcinoma

129
Q

Immediate management MI

A

MONA

Morphine
Oxygen therapy (if sats are less than 94%)
Nitrates
Aspirin + Antiplatelet

130
Q

Mechanism of action of beta agonists in asthma

A

e.g. salbutamol or salmeterol

Stimulation of G-protein coupled receptor causes smooth muscle relaxation and hence bronchodilation

131
Q

Mechanism of action of antimuscarinics in asthma

A

e.g ipratropium bromide

competitive inhibitor of acetylcholine
muscarinic receptors = parasympathetic effects e.g. bronchoconstriction
blocking these receptors causes the opposite effect and result in bronchodilation (sympathetic response)

132
Q

1st line test coeliac disease

A

Tissue transglutaminase (TTG) antibodies (IgA)

Remember you also need to look for selective IgA deficiency (endomyseal antibody)

133
Q

Gold standard investigation for coeliac disease

A

Endoscopic intestinal biopsy

134
Q

Biopsy findings coeliac disease

A

Villous Atrophy
Crypt Hyperplasia
Increase in intraepithelial lymphocytes

135
Q

Key signs of gastric cancer (3)

A

Dysphagia + palpable mass in abdomen + ascites

136
Q

Chronic heart failure: NYHA classification

A

1: no symptoms + no limitations
2: mild symptoms + comfortable at rest but ordinary activity = symptomatic
3: moderate symptoms + comfortable at rest but less than ordinary activity = symptomatic
4: severe symptoms + symptoms even at rest

137
Q

Management if BNP is ‘high’ when investigating HF

A

Transthoracic doppler echo within 2 weeks

’raised’ = transthoracic doppler echo within 6 weeks

138
Q

1st line investigation heart failure

A

NT-proBNP

139
Q

Radiological findings in HF

A

ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe veins
Pleural effusion

140
Q

Key treatment for acute pulmonary oedema (acute heart failure)

A

IV loop diuretics e.g. furosemide

141
Q

1st line therapy chronic heart failure

A

ACE inhibitor and beta blocker e.g. ramipril and bisoprolol

142
Q

2nd line therapy chronic heart failure

A

Aldosterone antagonist e.g. spironolactone
SGLT-2 inhibitors e.g. dapagliflozin

143
Q

AUDIT-C score

A

3 Qs:

How often do you have a drink containing alcohol?
How many units of alcohol do you drink on a typical day when you are drinking?
How often have you had 6 or more units (female) / 8 or more units (male), on a single occasion in the last year?

144
Q

When should you double your dose of hydrocortisone in adrenal insufficiency

A

temperature of > 38.0 degrees
cold, flu, diarrhoea or other infection
break a bone

145
Q

IBS presentation

A

Abdominal pain relieved by defecation
Bloating
Change in bowel habit

+ Made worse by stress, menstruation

146
Q

IBS pain relief

A

Buscopan (antispasmodic)

147
Q

C diff management

A

Metronidazole

148
Q

Charcot’s triad

A

Cholangitis: RUQ pain, jaundice, and fever

Cholecystitis = jaundice is absent

149
Q

Most common cause of cholecystitis

A

Gallstones

150
Q

Biliary colic vs other gallstone related conditions

A

No fever and LFTs/inflammatory markers are normal

151
Q

Gallstones risk factors

A

4 F’s
Fat
Female
Fertile
Fourty

+ Crohn’s, DM, rapid weight loss, drugs (COC)

152
Q

Management biliary colic

A

Elective laparoscopic cholecystectomy

153
Q

common bacteria which are causative of COPD exacerbations

A

Moraxella catarrhalis
Haemophilus influenzae
Strep pneumoniae

154
Q

Differentiating acute bronchitis from pneumonia

A

Hx: absent in acute bronchitis: sputum, wheeze, breathlessness

O/E: absent in acute bronchitis: no other focal chest signs (dullness to percussion, crepitations, bronchial breathing), systemic features (malaise, myalgia, fever)

155
Q

Management acute bronchitis

A

Supportive (analgesia, good fluid intake)

Antibiotic therapy: if the patient is systemically very unwell, pre-existing co-morbidities, high CRP
* 1st line = doxycycline (unless pregnant or a child)
* 2nd line = amoxicillin

156
Q

3 key points children’s influenza vaccine

A

It’s given intranasally
First dose is given at 2-3 years then annually after that
It is a live vaccine

157
Q

Contraindications to intranasal flu vaccine in children

A

Immunosuppressed
Aged < 2 years
Current febrile illness or blocked nose
Current wheeze or history of severe asthma
Egg allergy
Aspirin (e.g. Kawasaki)

inactivated, injectable vaccine given

158
Q

Who receives the annual influenza vaccine

A

All people over 65
Chronic disease
Diabetes Mellitus
Immunosuppression
Pregnant women

inactivated vaccine so cannot cause influenza

159
Q

Majority of hiatus hernia types

A

Sliding (GI junction moves above the diaphragm)

160
Q

Risk factors hiatus hernia

A

Obesity
Increased abdominal pressure e.g. ascites, multiparity

161
Q

Features of a hiatus hernia (4)

A

Heartburn
Dysphagia
Regurgitation
Chest pain

162
Q

Hiatus hernia investigation

A

1st line: endoscopy

Most sensitive: Barium swallow

163
Q

Management of hiatus hernia

A

All patients benefit from conservative management e.g. weight loss
Medical management: PPI therapy

164
Q

External haemorrhoids

A

Originate below the dentate line
Prone to thrombosis, may be painful

165
Q

Internal haemorrhoids

A

Originate above the dentate line
Do not generally cause pain

166
Q

Grading of internal haemorrhoids

A

I: do not prolapse
II: prolapse on defecation
III: manually reduced
IV: cannot be reduced

167
Q

Management of haemorrhoids

A

GP:
Soften stools (increase dietary fibre and fluid intake)
Topical local anaesthetics and steroids

Outpatient:
Rubber band ligation (1st) or injection sclerotherapy

168
Q

GORD management

A

PPI (-prazole) for 1 month (full dose)

  • If response, low dose treatment of PPI as required
  • If no response:
    Endoscopically proven oesophagitis: double dose PPI for 1 month
    Endoscopically negative reflux disease: H2RA or prokinetic for one month
169
Q

Complications of GORD

A

Oesophagitis
Ulcers
Anaemia
Barrett’s oesophagus
Oesophageal carcinoma

170
Q

Risk factors for developing GORD

A

Stress and anxiety
Smoking and alcohol
Coffee and chocolate (reduce LOS tone)
Obesity

171
Q

Features of fibromyalgia

A

Chronic pain (multiple site, sometimes all over)
Lethargy
Cognitive impairment (fibro fog)
Sleep disturbance, headaches, dizziness

172
Q

4 points on fibromyalgia management

A

Explanation
Aerobic exercise
CBT
Medication (pregabalin, duloxetine, amitriptyline)

173
Q

Early features of Lyme disease (within 30 days)

A

Erythema migrans (‘Bulls-eye’ rash at site of tick bite), usually painless - pathognomic

Systemic features

174
Q

Management of asymptomatic tick bites

A

Remove tick, no antibiotic treatment routinely recommended

175
Q

Management of suspected/confirmed Lyme disease

A

Doxycycline

176
Q

Polymyalgia rheumatica key features

A

Typical patient > 60 years old
Usually rapid onset (e.g. < 1 month)
Aching, morning stiffness in proximal limb muscles (weakness is not considered a symptom in polymyalgia)

Other: Mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats

177
Q

Investigations polymyalgia rheumatica

A

Raised inflammatory markers

Creatinine kinase and electromyography = normal

178
Q

Treatment polymyalgia rheumatica

A

Prednisolone

patients typically respond rapidly to steroids, failure to do so should prompt DDx

179
Q

Most important causative viral pathogen of COPD exacerbation

A

Human rhinovirus

180
Q

Features of COPD exacerbation

A

Increased dyspnoea, cough, wheeze
Increase in sputum (yellow-green)
Hypoxia / acute confusion
Fever
Cyanosis
Peripheral oedema

181
Q

Differentials COPD exacerbation

A

Pneumonia
Pneumothorax
Pleural effusion
Pulmonary embolism

182
Q

Management of COPD exacerbation (3)

A
  1. Increase frequency of bronchodilator (consider nebuliser)
  2. Prednisolone 30mg daily for 5 days
  3. Antibiotics: amoxicillin, clarithromycin, doxycycline (give Abx if sputum is purulent or clinical signs of pneumonia)
183
Q

Admission criteria for COPD exacerbation

A

Severe breathlessness
Acute confusion or impaired consciousness
Cyanosis
Oxygen saturation <90%
Social reasons (inability to cope at home)
Significant comorbidity (cardiac disease, insulin diabetes)

184
Q

thiazide-like diuretic examples

A

metolazone, indapamide, chlorthalidone

185
Q

Units of alcohol calculation

A

Vol (L) x % ABV

186
Q

Management of male with UTI

A

Nitrofurantoin for 7 days

187
Q

Atrial fibrillation 1st line rate control medication

A

beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem)

188
Q

Bacterial conjunctivitis presentation

A

Purulent discharge (eyes make be ‘stuck together’ in the morning)

189
Q

Viral conjunctivitis presentation

A

Serous discharge + recent URTI

190
Q

Management of infective conjunctivitis

A

Self limiting condition - settles without treatment within 1-2 weeks

1st line = Topical antibiotic therapy e.g. chloramphenicol drops (topical fusidic acid is used for pregnant women)

Contact lens should not be worn during an episode of conjunctivitis

School exclusion is not necessary

191
Q

Acute vs chronic anal fissure

A

Acute = less than 6 weeks
Chronic = more than 6 weeks

192
Q

3 risk factors for anal fissures

A

Constipation
IBS
STIs e.g. HIV, syphilis, herpes

193
Q

Presentation of anal fissures

A

Painful, bright red, rectal bleeding

194
Q

Management of an acute anal fissure

A

Soften stool: dietary advice (high fibre, high fluid), bulk-forming laxatives
Lubricants
Topical anaesthetics
Analgesia

195
Q

Chronic anal fissure management

A

Add to acute management: topical glyceryl trinitrate (GTN)

196
Q

Most common form of prostate cancer

A

Adenocarcinoma

197
Q

Other causes of raised PSA

A

Benign prostatic hyperplasia (BPH)
Prostatitis and UTI
Ejaculation
Vigorous exercise

198
Q

Management of low-grade prostate cancer

A

Active monitoring and watchful waiting

199
Q

Common complication of radical prostatectomy

A

Erectile dysfunction

200
Q

Complications of radiotherapy for prostate cancer (2)

A

Proctitis
Increased risk of bladder, colon and rectal cancer

201
Q

Classic triad reactive arthritis

A

Urethritis, conjunctivitis and arthritis

‘Can’t see, pee or climb a tree’

202
Q

Time course of reactive arthritis

A

Typically develops within 4 weeks of initial infection (symptoms generally last around 4-6 months)

203
Q

Most common STI associated with reactive arthritis

A

Chlamydia trachomatis

204
Q

Management of reactive arthritis

A

Symptomatic: analgesia, NSAIDs, intra-articular steroids

Methotrexate for persistent disease

205
Q

Common trigger for otitis externa

A

Recent swimming

206
Q

1st line treatment otitis externa

A

Topical antibiotics with or without steroid

if the patient fails to respond then refer to ENT

207
Q

End stage heart failure disease prognosis

A

High risk of dying within 6-12 months

208
Q

Raised urea and creatinine

A

Renal failure

209
Q

Blood tests to screen for alcohol dependence

A

Raised:
GGT
MCV
CDT

210
Q

Hypertension 4 further investigations

A

Creatinine
Electrolytes
ECG
Urinary protein

211
Q

4 causes of constipation

A

Advanced age
Inactivity
Low calorie intake
Low fibre diet
Medications
Female sex
Hypothyroidism

3a PTS - PM - ZTF (8 decks)

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