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C TO REVISE - PHASE 3A > GP CONDITIONS > Flashcards

GP CONDITIONS Flashcards

1
Q

HTN
What is malignant HTN?

A

Rapid rise in BP –
- Fibrinoid necrosis
- Retinal haemorrhages
- Papilloedema
- Exudates
Severe HTN ≥180/120

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2
Q

HTN
How might malignant HTN present?
Management?

A
  • Headache ± visual loss, typically younger + black patients
  • Same day specialist referral if Sx if not Ix for end-organ damage
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3
Q

HTN
After a diagnosis of HTN what other investigations would you do?

A
  • QRisk 3 + check for end-organ damage:
    – Urine dipstick (proteinuria + haematuria
    – Fundoscopy for hypertensive retinopathy
    – 12 lead ECG
    – First urine albumin creatinine ratio (ACR)
  • blood tests: HbA1c, U+Es, creatinine, cholesterol
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4
Q

HTN
In terms of clinical and ABPM/HBPM, how would you diagnose…

i) stage 1 HTN?
ii) stage 2 HTN?
iii) severe HTN?

A

i) ≥140/90 or ≥135/85
ii) ≥160/100 or ≥150/95
iii) ≥180 or ≥110 (clinical)

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5
Q

HTN
In terms of medication, what is first line treatment for…

i) 45 + T2DM?
ii) <55y/o?
iii) ≥55y/o?
iv) Afro-Caribbean?

A

i) ACEi or ARB
ii) ACEi or ARB
iii) CCB
iv) CCB

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6
Q

HTN
In terms of HTN medication, what is…

i) step 2?
ii) step 3?
iii) step 4?

A

i) The alternative (ACEi/ARB or CCB)
ii) Diuretics - Bendroflumethiazide, furosemide
iii) Beta-blocker, alpha-blocker, spironolactone if low potassium

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7
Q

HTN
What is an example and mechanism of action of ACEi?

A

Ramipril,

inhibit conversion of angiotensin I>II

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8
Q

HTN
What are the side effects of ACEi?

A

Dry cough + rash (bradykinin),
hypotension,
hyperkalaemia,
AKI (check renal function 1-2w after starting)
teratogenic

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9
Q

HTN
What are the clinical + ABPM/HBPM HTN treatment targets for…

i) <80?
ii) >80?
iii) diabetics?

A

i) <140/90 or <135/85
ii) <150/90 or <145/85
iii) <130/80

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10
Q

ANGINA
What is the secondary prevention of angina?

A

4As –
- Aspirin 75mg OD (+ second antiplatelet like clopidogrel for 12m)
- Atorvastatin 80mg ON
- Atenolol (or bisoprolol) titrated to max tolerated
- ACEi (ramipril) titrated to max tolerated

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11
Q

ANGINA
What are some long-term symptomatic relievers of angina?

A
  • Beta-blocker (in secondary prevention)
  • CCB (amlodipine)
  • Long-acting nitrates (isosorbide mononitrate)
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12
Q

ACS
What are the complications following ACS?

A

DREAD –
- Death
- RUpture of heart septum or papillary muscles
- oEdema
- Arrhythmia or Aneurysm
- Dressler’s syndrome

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13
Q

ACS
What is the management of NSTEMI?

A

BATMAN
– Beta-blocker
– Aspirin 300mg
– Ticagrelor 180mg
– Morphine
– Anticoagulant (LMWH)
– Nitrates (GTN)

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14
Q

ACS
What is the secondary prevention of ACS?

A

5As:
– Aspirin 75mg OD
– Another antiplatelet (clopidogrel or ticagrelor for 12m post PCI to prevent thrombus on stent)
– Atorvastatin 80mg ON
– ACEi
– Atenolol (or bisoprolol)

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15
Q

COPD
What are steps 1 and 2 of the COPD management?

A
  • 1 = SABA or SAMA
  • 2:
    – FEV1>50% = LABA and/or LAMA
    – FEV1 <50% LABA + ICS and/or LAMA (also offered in those with asthma/atopic features)
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16
Q

PNEUMONIA
What score can be used to assess severity of CAP?
How does this guide your management?

A
  • Confusion
  • Urea >7mmol/L
  • RR ≥30/min
  • BP <90 or 60
  • 65 ≤ age
  • 0-1 = PO amoxicillin in community
  • 2 = PO amoxicillin + clarithromycin in hospital
  • ≥3 = severe IV co-amoxiclav + clarithromycin ?ICU
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17
Q

CONSTIPATION
What is the management of constipation?

A
  • Hydration + increased fibre
  • Bulking agents = increased faecal mass + peristalsis (ispaghula husk)
  • Osmotic = retain fluid in bowel (lactulose)
  • Stimulant = increased intestinal motility (Senna)
  • Phosphate enemas
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18
Q

GALLSTONES
What causes gallstones?
Risk factors?

A
  • Imbalance between cholesterol + bile salts (75% mixed, 20% large yellow cholesterol, 5% bilirubinate)
  • Fat, Female, Forty, Fertile
  • Crohn’s as malabsorption of bile salts from terminal ileum
  • Haemolytic anaemias as increased bilirubin > bilirubinate stones
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19
Q

ACUTE CHOLECYSTITIS
What is the clinical presentation of acute cholecystitis?

A
  • RUQ pain radiating to tip of scapula
  • FEVER (differentiates from biliary colic), N+V
  • Murphy’s sign = tenderness worse on inspiration with 2 fingers on RUQ
  • NO jaundice (differentiates from ascending cholecystitis)
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20
Q

ACUTE CHOLECYSTITIS
Investigations for acute cholecystitis?

A
  • FBC (raised WCC), LFTs,
  • USS shows gallstones + distended gallbladder with thickened wall
  • Sonographic murphy’s
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21
Q

ACUTE CHOLECYSTITIS
Management of acute cholecystitis?

A
  • Conservative = NBM, IV fluids, pain relief, IV Abx
  • Lap chole
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22
Q

PERIPHERAL VASCULAR DISEASE
what are the investigations for PVD?

A

1st line = ankle brachial pressure index (ABPI), duplex ultrasound

<0.3 = critical ischaemia

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23
Q

ARRHYTHMIAS
Give 2 effects of hypokalaemia on an ECG

A
  1. Flat T waves
  2. QT prolongation
  3. ST depression
  4. Prominent U waves
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24
Q

ARRHYTHMIAS
Give an effect of hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
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25
Q

ARRHYTHMIAS
Give an effect of hypercalcaemia on an ECG

A
  1. QT shortening
  2. Tall T wave
  3. No P waves
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26
Q

ARRHYTHMIAS
What ECG changes might you see with someone with ventricular tachycardia?

A

Crescendo-decrescendo amplitude = torsades de pointes

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27
Q

HEART BLOCK
Describe a first degree heart block

A

Fixed prolongation of the PR interval due to delayed conduction to the ventricles
- PR interval >0.22s
- asymptomatic

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28
Q

HEART BLOCK
Describe a second degree heart block

A

There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles

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29
Q

HEART BLOCK
Describe a Mobitz type 1 second degree heart block

A

PR interval gradually increases until AV node fails and no QRS is seen
PR interval returns to normal and the cycle repeats

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30
Q

HEART BLOCK
Describe a Mobitz type 2 second degree heart block

A

Sudden unpredictable loss of AV conduction and so loss of QRS
PR interval is constant but every nth QRS is missing
wide QRS

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31
Q

HEART BLOCK
Explain the pathophysiology of a BBB

A

Lack of simultaneous ventricular contractions
LBBB = R before L
RBBB = L before R

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32
Q

IBS
Describe the pharmacological treatment of IBS

A
  1. Antispasmoidics for bloating - mebeverine
  2. Laxatives for constipation
  3. Anti-motility agent for diarrhoea - loperamide
  4. Tricyclic antidepressants
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33
Q

HTN
What is an example and mechanism of action of CCB?

A

Amlodipine,

act on L-type Ca2+ channels

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34
Q

HTN
What is an example and mechanism of action of thiazide-like diuretic?

A

Indapamide,

locks Na+ reabsorption at DCT by blocking Na+/Cl- symporter

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35
Q

HTN
What is an example and mechanism of action of ARB?

A

Candesartan,

blocks effects of angiotensin II at the AT1 receptor

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36
Q

HTN
What are the side effects of CCB?

A

Oedema,
headache,
flushing
palpitations

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37
Q

HTN
Name 4 classes of diuretics

A
  1. Thiazides
  2. Loop
  3. Potassium sparing
  4. Aldosterone antagonists
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38
Q

HTN
What are the side effects of beta-blocker?

A

Headache,
hypotension,
erectile dysfunction

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39
Q

HTN
What are the risk factors for HTN?

A

Modifiable:
- alcohol intake
- sedentary lifestyle
- diabetes mellitus
- sleep apnoea
- smoking

Non-modifiable:
- Increasing age
- family history
- ethnicity - afro-Caribbean

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40
Q

HTN
Where in the kidney do thiazide diuretics work?

A

The distal tubule

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41
Q

ACS
Give 3 signs of MI

A
  1. Hypo/hypertension
  2. 3rd/4th heart sound
  3. Signs of congestive heart failure
  4. Ejection systolic murmur
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42
Q

ACS
How does aspirin work?

A

Antiplatelet
Irreversibly inhibits COX –> reduced thromboxane 2 synthesis –> platelet aggregation reduced

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43
Q

ACS
How does clopidogrel work?

A

Antiplatelet
P2Y12 inhibitor –> prevents platelet activation

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44
Q

OTITIS EXTERNA
What is malignant otitis externa?

A
  • Immunocompromised, DM or elderly where it can spread to the surrounding bones (mastoid + temporal)
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45
Q

OTITIS EXTERNA
What are some causes of otitis externa?

A
  • Infection (staph. aureus, pseudomonas aeruginosa or fungal)
  • Seborrhoeic dermatitis
  • Contact dermatitis (allergic + irritant)
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46
Q

OTITIS EXTERNA
What is the management of otitis externa?

A
  • May need to clean ear canal first with syringing or irrigation
  • Topical Abx or a combined topical Abx with steroid = 1st line
  • PO flucloxacillin if infection spreading, swab before
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47
Q

T2DM
What is the pathophysiology of T2DM?

A
  • Repeated exposure to glucose + insulin = resistance to effects of insulin so more required for a response
  • Beta cells fatigued + damaged so produce less
  • Low insulin + peripheral insulin resistance = impaired glucose tolerance
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48
Q

T2DM
What values are diagnostic for T2DM?

A
  • HbA1c ≥48mmol/mol Dx
    1 result if Sx, 2 separate if none:
  • Random glucose ≥11.1mmol/L
  • Fasting glucose ≥7mmol/L
  • OGTT 2h ≥11.1mmol/L
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49
Q

T2DM
What is a main complication of uncontrolled T2DM?

A
  • Hyperglycaemic hyperosmolar state
  • Decrease insulin = increase serum glucose + serum osmolality + urination but no ketosis as still some endogenous insulin
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50
Q

T2DM
How does HHS present?
How is it diagnosed?
Management?

A
  • Marked dehydration (polydipsia, polyuria, hypovolaemia) + impaired consciousness
  • Plasma glucose >30mmol/L, plasma osmolality >320mOsm
  • IV fluid replacement, infuse insulin, LMWH prophylaxis as hyperviscous blood
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51
Q

T2DM
List 6 medications that can be used in T2DM

A
  • Metformin (biguanide, first line)
  • Gliclazide (sulfonylurea)
  • Sitagliptin (DPP4 inhibitor)
  • Empagliflozin (SGLT)
  • Glitazone (pioglitazone)
  • GLP-1 mimetics
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52
Q

T2DM
What is the mechanism of action of…

i) metformin?
ii) gliclazide?
iii) sitagliptin?

A

i) Increased insulin sensitivity, reduced gluconeogenesis in liver + helps weight
ii) Stimulates beta cells to secrete insulin
iii) Increases incretin levels which inhibit glucagon production

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53
Q

T2DM
What is the mechanism of action of…

i) empagliflozin?
ii) glitazone?
iii) GLP-1 mimetics?

A

i) Blocks glucose reabsorption in PCT of kidneys + promotes excretion of excess glucose in urine
ii) Increases insulin sensitivity + decreases liver production of glucose
iii) Incretin (GLP-1) mimetic inhibits glucagon secretion (after triple therapy)

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54
Q

T2DM
What are some side effects of…

i) metformin?
ii) gliclazide?
iii) sitagliptin?
iv) empagliflozin?
v) glitazone?
vi) GLP-1 mimetics?

A

i) GI upset (D+V, abdo pain), lactic acidosis
ii) Hypoglycaemia + weight gain
iii) GI upset, pancreatitis
iv) Glucosuria, weight loss + UTI risk
v) Weight gain, fluid retention, heart failure
vi) Weight loss, N+V, pancreatitis

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55
Q

HYPERTHYROIDISM
What are the 3 mechanisms explaining the causes of hyperthyroidism?

A
  • Overproduction of thyroid hormone
  • Leakage of pre-formed hormone from thyroid
  • Ingestion of excess thyroid hormone
56
Q

HYPERTHYROIDISM
What are some other causes of hyperthyroidism?

A
  • Toxic multinodular goitre = nodules secrete excess thyroid hormones (elderly women)
  • Toxic adenoma = solitary nodule producing T3/4
  • DeQuervain’s thyroiditis = acute inflammation
  • Exogenous iodine (food, amiodarone)
57
Q

HYPERTHYROIDISM
What are the Graves’ disease specific features?

A
  • Diplopia, ophthalmoplegia, increased tears
  • Exophthalmos, lid lag + retraction
  • Thyroid acropachy (clubbing, painful digits)
  • Pretibial myxoedema
58
Q

HYPERTHYROIDISM
What are some investigations for hyperthyroidism?

A
  • TFTs (primary = low TSH, high T3/4, secondary = high TSH, high T3/4 hypothalamus or pituitary pathology)
  • Thyroid autoantibodies
  • Isotope scan
59
Q

HYPERTHYROIDISM
What is the management of hyperthyroidism?

A
  • Beta-blockers for rapid sympathetic control (propranolol)
  • Carbimazole 1st line, propylthiouracil 2nd
  • Radioiodine therapy
  • Surgical thyroidectomy
  • NSAIDs + beta-blockers for self-limiting DeQuervain’s
60
Q

HYPOTHYROIDISM
What are some investigations for hypothyroidism?

A
  • TFTs = primary (high TSH, low T3/4), secondary (low TSH, low T3/4)
  • Thyroid peroxidase antibody (TPO-Ab) + anti-thyroglobulin in Hashimoto’s
  • Anti-TSH positive + TPO in atrophic thyroiditis
61
Q

OSTEOARTHRITIS
What bony swellings may be seen in osteoarthritis?

A
  • Distal IPJ = Heberden’s nodes
  • Proximal IPJ = Bouchard’s nodes
  • Squaring at base of thumb at carpometacarpal joint (saddle joint used in many activities so prone to wearing)
62
Q

OSTEOARTHRITIS
What would plain radiograph show in osteoarthritis?

A

LOSS –
- Loss of joint space
- Osteophytes
- Subarticular sclerosis (increased density of bone along joint line)
- Subchondral cysts (fluid filled holes in the bone)

63
Q

OSTEOARTHRITIS
What medical treatment may be given for osteoarthritis?

A
  • Regular PO + topical NSAIDs
  • PO NSAIDs (?+PPI) for intermittent use
  • ?Opiates like codeine + morphine
  • Intra-articular steroid injections to reduce inflammation
64
Q

GOUT
What are some causes of gout?
Who is it most common in?

A
  • Increased uric acid production = chemo, pyrazinamide
  • Decreased uric acid excretion = diuretics, renal impairment, alcohol excess
  • Older men
65
Q

GOUT
What are some risk factors for gout?
What are some factors that may precipitate an attack?

A
  • Alcohol, high purine diet (red meat + seafood), cell damage + Death (surgery, chemo)
  • Dietary excess, diuretics, dehydration, sepsis
66
Q

GOUT
What is the management for gout for…

i) an acute flare?
ii) long-term prophylaxis?

A

i) NSAIDs like ibuprofen first line (unless C/I), colchicine second line (inhibits mitosis but SEs of diarrhoea), steroids last
ii) Allopurinol (xanthine oxidase inhibitor but start after acute attack settled in about 2w)

67
Q

PSEUDOGOUT
What is the management of pseudogout?

A
  • NSAIDs, colchicine
  • Intra-articular steroids or PO
  • Joint aspiration of arthrocentesis if severe
68
Q

PMR
What is the management of PMR?

A
  • ESR/CRP raised, CK normal
  • PO prednisolone shows dramatic response (diagnostic)
69
Q

B12/PERNICIOUS ANAEMIA
What are the B12 specific features of the anaemia?

A
  • Peripheral neuropathy with numbness or paraesthesia
  • Loss of vibration sense or proprioception
  • Visual, mood or cognitive changes
  • Glossitis = beefy-red sore tongue
70
Q

B12/PERNICIOUS ANAEMIA
What is the management of B12/pernicious anaemia?

A
  • PO B12 (cyanocobalamin) if dietary origin
  • IM hydroxocobalamin if pernicious
  • Do NOT give folate as can cause subacute combined degeneration of cord = distal sensory loss, ataxia + mixed UMN/LMN signs
71
Q

ARRHYTHMIAS
Give 3 effects hyperkalaemia on an ECG

A

GO - absent P wave
GO TALL - tall T wave
GO long - prolonged PR
GO wide - wide QRS

72
Q

TYPE 2 DIABETES
Describe the pathophysiology of T2DM

A

Insulin binds normally to its receptor – insulin resistance develops post-receptor

Circulating insulin levels are higher than in healthy patients but inadequate to restore glucose homeostasis
Increased glucose production in liver- inadequate suppression of gluconeogenesis and there’s reduced glucose uptake in peripheral tissues

Hyperglycaemia and lipid excess are toxic to beta cells - reduced beta cell mass

Don’t tend to develop ketoacidosis by do get glycosuria

73
Q

TYPE 2 DIABETES
Why is insulin secretion impaired in T2DM

A

Due to lipid deposition in the pancreatic islets

74
Q

TYPE 2 DIABETES
what are the risk factors for T2DM?

A

Increase w/ age
M > F
Ethnicity: African-Carribean, Black African and South Asian
Obesity
Hypertension

75
Q

TYPE 2 DIABETES
What happens to insulin resistance, insulin secretion and glucose levels in T2DM?

A

Insulin resistance increase
Insulin secretion decreases
Fasting and post-prandial glucose increase

76
Q

TYPE 2 DIABETES
Describe the treatment pathway for T2DM

A
  1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
  2. Metformin
  3. Metformin and sulfonylurea (GLICLAZIDE)
  4. Metformin + sulfonylurea (GLICLAZIDE) + insulin
  5. metformin +sulonylurea (GLICLAZIDE) + insulin +PIOGLITAZONE
  6. Increase insulin dose as required
77
Q

TYPE 2 DIABETES
How does metformin work in treating T2DM?

A

Increase insulin sensitivity and inhibits glucose production

78
Q

TYPE 2 DIABETES
How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

79
Q

TYPE 2 DIABETES
Give a potential consequence of taking Sulfonylurea for the treatment of T2DM

A

Hypoglycaemia

80
Q

REACTIVE ARTHRITIS
What investigations might you do in someone you suspect to have reactive arthritis?

A

ESR + CRP - raised
ANA - negative
RF - negative
X-ray - sacroiliitis or enthesopathy
Joint aspirate - negative (exclude septic arthritis + gout)

81
Q

REACTIVE ARTHRITIS
How is reactive arthritis treated?

A

NSAID
Corticosteroids
DMARD - chronic arthritis

82
Q

FIBROMYALGIA
What is the diagnostic criteria for fibromyalgia?

A

Chronic widespread pain lasting for > 3 months with other causes excluded
Pain is at 11/18 tender point sites for 6 months

83
Q

FIBROMYALGIA
Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
84
Q

FIBROMYALGIA
Give 3 disease that might be included in the differential diagnosis for fibromyalgia

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
85
Q

FIBROMYALGIA
Describe the management of fibromyalgia

A
  • Educate the patient and family
  • CBT and exercise programmes - reset pain thermostat
  • Acupuncture
  • Analgesics - tramadol, codeine
  • Low dose antidepressants (amitriptyline) and anticonvulsants (pregabalin)
86
Q

GOUT
Describe the pathophysiology of gout

A

Purine –> (by xanthine oxidase) xanthine –> uric acid –> monosodium rate crystals OR excreted by kidneys
Urate blood/tissue imbalance –> rate crystal formation –> inflammatory response through phagocytic activation

Overproduction/under excretions of uric acid causes build up and precipitated out in joints

87
Q

GOUT
Give 3 causes of gout

A

= Hyperuricaemia

  1. Impaired excretion - CKD, diuretics, hypertension
  2. Increased production - hyperlipidaemia
  3. Increased intake - high purine diet = red meat, seafood, fructose, alcohol
88
Q

PSEUDOGOUT
What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
89
Q

PSEUDOGOUT
What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

90
Q

GOUT
What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

91
Q

ACNE VULGARIS
what is the pathophysiology?

A

it is multifactorial
- follicular epidermal hyperproliferation resulting in the formation of a keratin plug. This in turn causes obstruction of the pilosebaceous follicle. Activity of sebaceous glands may be controlled by androgen, although levels are often normal in patients with acne

  • colonisation by the anaerobic bacterium Propionibacterium acnes
  • Inflammation
92
Q

BPH
What are some investigations for BPH?

A
  • DRE = smooth but enlarged prostate
  • U+Es, serum PSA (rise)
  • Urine dip + MC&S
  • International prostate symptom score (I-PSS) looks at LUTS + how much affect day-to-day life
  • Transrectal USS ± biopsy
  • Flexibly cystoscopy
93
Q

BPH
What 2 medications can be used in BPH and what is their mechanism of action?

A
  • Alpha blockers 1st line (doxazosin, tamsulosin) to relax prostate smooth muscle
  • 5-alpha reductase inhibitor (finasteride) which decreases prostate size by less conversion of testosterone into dihydrotestosterone
94
Q

BPH
What are the side effects of…

i) alpha blockers?
ii) 5-alpha reductase inhibitors?

A

i) Postural hypotension (vasodilation), dizziness, dry mouth
ii) Erectile dysfunction, reduced libido, ejaculation issues

95
Q

BPH
What surgical options may be considered for BPH?
Complications?

A
  • Transurethral resection of prostate (TURP)
  • SEs = urethral stricture, retrograde ejaculation, prostate perforation
  • Retropubic prostatectomy if very large (open surgery)
96
Q

CKD
How is CKD diagnosed?

A
  • eGFR < 60mL/min/1.73m2,
    or:
  • eGFR < 90mL/min/1.73m2 + signs of renal damage,
    or:
  • Albuminuria > 30mg/24hrs (Albumin:Creatinine > 3mg/mmol)
97
Q

CKD
What are the different stages of CKD?

A

Stage 1 = <90
Stage 2 = 60-89
Stage 3a = 45-59
Stage 3b = 30-44
Stage 4 = 15-29
Stage 5 = <15

98
Q

CKD
Briefly describe the pathophysiology begins CKD

A

Hyper-filtration for nephrons that work –> glomerular hypertrophy and reduced arteriolar resistance –> raised intraglomerular capillary pressure and strain –> accelerates remnant nephron failure (progressive)

99
Q

CKD
Name 4 cause of CKD

A
  1. DM - 24% of patients
  2. Hypertension
  3. Glomerulonephritis
  4. Congenital - polycystic kidney disease
  5. Urinary tract obstruction
  6. drugs - NSAIDs, ACEi, antidepressants, many antibiotics
100
Q

CKD
Give 3 signs of CKD

A

Often asymptomatic until very low kidney function

  • Fluid retention - oedema and raised JVP
  • Oliguria - 0.5 mL/kg/h or <500mL/day
  • Effects of uraemia
    pruritus = ureamic frost, yellow/grey complexion, nausea, reduced appetite
  • cardiac arrhythmias - hyperKa
    Fatigue, pallor - anaemia
  • Bone pain - hyperphosphatemia (CKD-MBD)
101
Q

CKD
Describe the management of CKD

A

treat underlying cause

Hypertension - ACEi / ARB…B-blocker…

Diabetes - metformin, pioglitazone, sulphonylurea

Anaemia - exogenous EPO, Fe sulfate

Oedema - fluid and sodium restriction, loop diuretic

CVD - aspirin, atorvostatin 20mg

CKD mineral bone disease - vit. D supplementation, low phosphate diet

dialysis, transplant

102
Q

PROSTATE CANCER
Define prostate cancer

A

Adenocarcinoma in the peripheral zone of the prostate gland

103
Q

PROSTATE CANCER
Where can prostate cancer metastasise to?

A

Lymph nodes and bone

Rarely = brain, liver, lung

104
Q

PROSTATE CANCER
What can cause prostate cancer?

A
  1. High testosterone levels

2. Family history - 2/3x increased risk if 1st degree relative is affected

105
Q

PROSTATE CANCER
What investigations might you do in someone who you suspect has prostate cancer?

A

Digital Rectal Exam and PSA are done in community,
Transrectal USS and biopsy = DIAGNOSTIC
Gleason grading system - higher the score the worse the prognosis

106
Q

PROSTATE CANCER
What grading system is used in prostate cancer?

A

Gleason grading = higher the score, the more aggressive the cancer

107
Q

PROSTATE CANCER
Other than prostate cancer, what can cause an elevated PSA?

A
  1. Benign prostate enlargement
  2. UTI
  3. Prostatitis
108
Q

UTI
Name 3 UTI causative organisms

A
  1. Uropathogenic strains of E. coli (UPEC) - 82%
  2. Coagulase negative staph (s. saprophyticus)
  3. Proteus mirabilis
  4. Enterococci
  5. Klebsiella pneumonia
109
Q

UTI
Give 4 risk factors of UTI’s

A
  1. Catheter
  2. Female
  3. Prostatic hypertrophy (obstructs)
  4. Low urine volume
  5. Urinary tract stones
  6. Pregnancy
110
Q

UTI
Give 3 host defence mechanisms against UTIs

A
  1. Antegrade flushing of urine
  2. Tamm-horsfall protein
  3. GAG layer
  4. Low urine pH
  5. Commensal flora
  6. Urinary IgA
111
Q

ACNE VULGARIS
what is the management?

A

step-wise management
1. single topical therapy (topical retinoids, benzoyl peroxide)
2. topical combination therapy ( topical abx, benzoyl peroxide, topical retinoids)
3. topical retinoid + COCP/oral antibiotics - tetracyclines, erythromycin in pregnancy/<12 years old (maximum 3 months)
4. oral isotretinoin - under specialist supervision only

112
Q

ACNE VULGARIS
what is a complication of long term antibiotics use and how can this be treated?

A

gram-negative folliculitis

treated with high dose trimethoprim

113
Q

LYME DISEASE
what is lyme disease caused by?

A

spirochaete Borrelia burgdorferi and is spread by tick

114
Q

LYME DISEASE
what are the early features of lyme disease?

A
  • erythema migrans - bulls eye rash, develops 1-4 weeks after bite, usually painless
  • headache
  • lethargy
  • fever
  • arthralgia
115
Q

LYME DISEASE
what are the later features of lyme disease?

A

CVS
- heart block
- peri/myocarditis

neurological
- facial nerve palsy
- radicular pain
- meningitis

116
Q

LYME DISEASE
what are the investigations?

A
  • diagnosed clinically if erythema migrans is present
  • ELISA test
  • immunoblot for lyme disease
117
Q

LYME DISEASE
what is the management?

A
  • doxycycline (amoxicillin if pregnant)
  • ceftriaxone in disseminated disease
118
Q

ANAPHYLAXIS
what is the emergency management?

A

500 micrograms IM adrenaline every 5 minutes

IV fluid bolus

119
Q

ANAPHYLAXIS
what is refractory anaphylaxis?

A

defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline

120
Q

ANAPHYLAXIS
what is the management of refractory anaphylaxis?

A

IV adrenaline infusion
IV fluid boluses
High flow oxygen

If no response to adrenaline try noradrenaline, vasopressin

121
Q

CONJUNCTIVITIS
what are the clinical features of viral conjunctivitis?

A
  • serous discharge
  • more likely to be unilateral
  • more common than bacterial
122
Q

CONJUNCTIVITIS
what is the management of viral conjunctivitis?

A

conservative
prevent spread - hand hygiene and don’t share towels
artificial tears

123
Q

CONJUNCTIVITIS
what are the clinical features of bacterial conjunctivitis?

A
  • purulent discharge
  • eyelids stuck together
124
Q

CONUNCTIVITIS
what are the causes of bacterial conjunctivitis?

A
  • staph. epidermis
  • staph. aureus
  • strep. pneumoniae
  • H. influenzae
  • chlamydia
  • gonorrhoea
125
Q

CONJUNCTIVITIS
what is the management of bacterial conjunctivitis?

A
  • resolves within 7-14 days
  • topical chloramphenicol
  • lubricating eye drops
126
Q

BURSITIS
what are the symptoms?

A

Affected joint might:
- feel achy or stiff
- hurt more when moved or press on it
- look swollen and red

127
Q

BURSITIS
what are the causes?

A

Repetitive movements that put pressure on the bursae
- throwing a baseball or lifting over head repeatedly
- leaning on elows for long periods
- extensive kneeling

other causes include trauma, RA, gout and infection

128
Q

BURSITIS
what are the risk factors?

A
  • age
  • occupation
  • systemic conditions such as RA, gout and DM
  • obesity
129
Q

BURSITIS
how can it be prevented?

A
  • use kneeling pads
  • lift properly
  • take frequent breaks
  • weight loss
  • exercising
130
Q

BURSITIS
what are the investigations?

A
  • clinical diagnosis
  • x-ray
  • USS or MRI
  • FBC with CRP, ESR
131
Q

BURSITIS
what is the management?

A
  • anti-inflammatory - NSAIDs
  • antibiotics for infection
  • physiotherapy
  • corticosteroid injections
  • crutches to relieve pressure
  • surgical drainage
132
Q

FOLLICULITIS
what are the causes?

A
  • staph aureus infection

can also be caused by viruses, fungi, parasites medications or physical injury

133
Q

FOLLICULITIS
what are the risk factors?

A
  • wearing clothes that trap heat/sweat
  • using hot tub/pool
  • causing damage to hair follicles through shaving, waxing etc
  • medications - corticosteroids, acne treatmetn, chemotherapy
  • having dermatitis or hyperhidrosis
  • having DM, HIV/AIDS
134
Q

FOLLICULITIS
what is the management?

A
  • antibiotic lotion
  • antifungal shampoos
  • creams to calm inflammation
135
Q

BENIGN EYELID DISORDERS - BLEPHARITIS
what are the causes?

A

Atopic dermatitis (staphylococcal)
Seborrheic dermatitis
Acne rosacea
Demodex infestation (mites)

136
Q

BENIGN EYELID DISORDERS - BLEPHARITIS
what is the management?

A

lid hygiene
- warm compression, eyelid massage, cleaning eyelids

topical antibiotic ointment
low dose tetracyclines
regular omega-3 supplements

C TO REVISE - PHASE 3A (11 decks)

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