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My Phase 3a Revision > GP - RENAL, DERM, MSK, ENDOCRINE & INFECTION > Flashcards

GP - RENAL, DERM, MSK, ENDOCRINE & INFECTION Flashcards

1
Q

OTITIS EXTERNA
What is otitis externa?
What is it associated with?

A
  • Inflammation of external ear canal
  • Swimmer’s ear as associated with frequent swimming
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2
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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3
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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4
Q

OTITIS EXTERNA
What is the clinical presentation of otitis externa?

A
  • Ear pain (mild), itchy + discharge common, ?hearing loss
  • Otoscopy = red, swollen or eczematous canal
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5
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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6
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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7
Q

T2DM
What are some causes of T2DM?
How does it present?

A
  • Genetics + environment (FHx, obesity, poor diet)
  • Asian, men, older age
  • No Sx but sometimes polyuria, polydipsia, lethargy, visual blurring
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8
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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9
Q

T2DM
What values suggest…

i) impaired fasting glucose?
ii) impaired glucose tolerance?

A

i) 6.1-6.9mmol/L
ii) 7.8-11.1mmol/L

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10
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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11
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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12
Q

T2DM
What is the first line management of T2DM?
What are the HbA1c targets in T2DM?

A
  • Lifestyle advice = exercise, less carbs/fat, smoking cessation
  • <48mmol/mol for new pts or <53 if on ≥2 Tx
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13
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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14
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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15
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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16
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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17
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
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18
Q

HYPERTHYROIDISM
What is the most common cause of hyperthyroidism?
What is the pathophysiology?

A
  • Graves’ disease
  • Autoimmune induced excess production of thyroid hormone, esp T3
  • TSH receptor stimulating antibody (TRAb, IgG), autoimmune link to T1DM, coeliac, Addison’s
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19
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)
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20
Q

HYPERTHYROIDISM
What are the general signs and symptoms of hyperthyroidism?

A
  • Anxiety, irritability
  • Sweating, palpitations (?AF), tremor, tachycardia
  • Heat intolerance
  • Weight loss, increased appetite, diarrhoea
  • Oligomenorrhoea
  • Thin hair, warm skin
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21
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
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22
Q

HYPERTHYROIDISM
How would De Quervain’s thyroiditis present?

A
  • PAIN in de QuerVAIN = tender goitre, fever, dysphagia (viral infection)
  • Hyperthyroid phase > hypothyroid phase (TSH falls due to -ve feedback)
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23
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
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24
Q

HYPERTHYROIDISM
What is a complication of hyperthyroidism?
Management?

A
  • More severe presentation with pyrexia, tachycardia + delusion
  • Admission, supportive (fluid resus), beta-blockers, ?anti-arrhythmic
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25
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
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26
Q

HYPERTHYROIDISM
What are the 2 methods for administering anti-thyroid drugs?
What are side effects of them?

A
  • Titration
  • Block + replace (block all production + take levothyroxine)
  • Carbimazole = agranulocytosis
  • Propylthiouracil = severe hepatic reactions
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27
Q

HYPERTHYROIDISM
What are some risks with…

i) radioiodine therapy?
ii) surgical thyroidectomy?

A

i) C/I in pregnancy, breastfeeding + may leave patient hypothyroid
ii) Risk to recurrent laryngeal nerve (hoarse voice) + hypoparathyroidism

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28
Q

HYPOTHYROIDISM
What are some common causes of hypothyroidism?

A
  • Primary autoimmune (atrophic thyroiditis, Hashimoto’s thyroiditis)
  • Iodine deficiency (#1 worldwide)
  • Secondary to carbimazole, radioactive iodine, thyroidectomy, lithium + amiodarone
  • Central causes like hypopituitarism (Sheehan’s, tumours, radiation)
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29
Q

HYPOTHYROIDISM
What is…

i) atrophic thyroiditis?
ii) Hashimoto’s thyroiditis?

A

i) Diffuse lymphocytic infiltration of thyroid leading to atrophy + so no goitre
ii) Goitre due to lymphocytic + plasma cell infiltration, #1 cause in developed world

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30
Q

HYPOTHYROIDISM
What are some symptoms of hypothyroidism?

A
  • Weight gain, decreased appetite + constipation
  • Cold intolerance
  • Lethargy, menorrhagia
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31
Q

HYPOTHYROIDISM
What are some signs of hypothyroidism?

A

BRADYCARDIC
- Bradycardia
- Reflexes relax slowly
- Ataxia
- Dry, thin hair/skin
- Yawning
- Cold hands
- Ascites
- Round puffy face
- Defeated demeanour
- Immobile
- CHF

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32
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
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33
Q

HYPOTHYROIDISM
What is the management of hypothyroidism?
Prescribing information?

A
  • Lifelong levothyroxine to replace (titrate up)
  • 30m before breakfast as iron decreases absorption of thyroxine
  • Repeat TFTs monthly until stable
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34
Q

GALLSTONES
What is the clinical presentation of gallstones?

A
  • Severe RUQ may radiate to tip of scapula
  • N+V
  • May be triggered by heavy, fatty meal
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35
Q

OSTEOARTHRITIS
What is osteoarthritis?

A
  • Non-inflammatory wear + tear arthritis
  • Destruction of articular cartilage makes exposed subchondral bone sclerotic > increases vascularity + subchondral cysts form where repair produces cartilaginous growth from chondrocytes which calify (osteophytes)
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36
Q

OSTEOARTHRITIS
What causes osteoarthritis?
Risk factors?

A
  • Secondary OA can occur in joints due to congenital disease + damage
  • Obesity, increasing age, trauma, female, FHx, occupation (manual labour)
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37
Q

OSTEOARTHRITIS
What are the main symptoms of osteoarthritis?

A
  • Morning stiffness <30m
  • Stiffness after rest (gelling)
  • Bony swellings/joint deformities
  • Reduced ROM, weak grip + reduced functioning
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38
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)
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39
Q

OSTEOARTHRITIS
What joints may be affected in osteoarthritis?

A
  • Hips, knees, sacroiliac joints, MCP joint at base of thumb (squaring), wrist, cervical spine
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40
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)

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41
Q

OSTEOARTHRITIS
What is the conservative management of osteoarthritis?

A
  • Education
  • Lifestyle (weight loss)
  • Physio to improve strength
  • Orthotics to support activities + function (walking aids)
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42
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
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43
Q

OSTEOARTHRITIS
What surgery may be offered in osteoarthritis?

A
  • Arthroscopy for loose bodies (can cause locking e.g. knee)
  • Osteotomy (changing bone length)
  • Arthroplasty (joint replacement, risk of infection)
  • Fusion (often ankle + foot)
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44
Q

GOUT
What is gout?
Pathophysiology?

A
  • Inflammatory arthritis due to hyperuricaemia + intra-articular monosodium urate crystals
  • Urate derived from breakdown of purines (adenine + guanine)
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45
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
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46
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
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47
Q

GOUT
How does gout present?

A
  • Acute hot, swollen + painful joints (exclude septic)
  • Wrists, base of thumb (carpometacarpal joint) + metatarsophalangeal joint of big toe
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48
Q

GOUT
What are some signs of gout?

A
  • Chronic tophaceous gout = tophi (s/c deposits of urate crystals in skin + joints, often small joints of hands, elbows, ear)
  • Chronic polyarticular gout = painful erythematous swelling
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49
Q

GOUT
What investigations would you do for gout?

A
  • Serum urate elevated
  • Joint fluid aspiration MC&S = no bacteria, Needle shaped crystals with Negative birefringent under polarised light
  • XR = joint space maintained, lytic bone lesions, punched out erosions
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50
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)

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51
Q

PSEUDOGOUT
What is pseudogout?
What is it associated with?

A
  • Microcrystal synovitis due to deposits of calcium pyrophosphate crystals
  • Hyperparathyroid, hypothyroid, haemochromatosis, hypophosphataemia
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52
Q

PSEUDOGOUT
How does pseudogout present?

A
  • Acute hot, swollen + stiff joints
  • Monoarthropathy affecting shoulders, wrists + knees
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53
Q

PSEUDOGOUT
What are the investigations for pseudogout?

A
  • Joint fluid aspiration MC&S = no bacteria, Rhomboid shaped crystals with Positive birefringent under polarised light
  • XR = may show soft tissue calcium deposition (chondrocalcinosis) = thin white line in middle of joint space
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54
Q

PSEUDOGOUT
What is the management of pseudogout?

A
  • NSAIDs, colchicine
  • Intra-articular steroids or PO
  • Joint aspiration of arthrocentesis if severe
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55
Q

PMR
What is polymyalgia rheumatica (PMR)?
Associations?

A
  • Inflammatory condition (vasculitis) causing pain + stiffness in shoulder, pelvic girdle + neck
  • GCA
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56
Q

PMR
What is the clinical presentation of PMR

A
  • Bilateral shoulder pain, may radiate to elbow
  • Bilateral pelvic girdle pain
  • Worse with movement + sleep interference
  • Morning stiffness ≥45m
  • Systemic Sx = weight loss, fatigue, low grade fever
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57
Q

PMR
What is the management of PMR?

A
  • ESR/CRP raised, CK normal
  • PO prednisolone shows dramatic response (diagnostic)
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58
Q

B12/PERNICIOUS ANAEMIA
What is the pathophysiology of B12 deficiency?

A
  • Absorption of B12 in terminal ileum + intrinsic factor (via gastric parietal cells) dependent for transport across intestinal mucosa
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59
Q

B12/PERNICIOUS ANAEMIA
What are some causes of B12 deficiecny?

A
  • Autoimmune (pernicious) = atrophic gastritis leading to destruction of parietal cells in stomach > less intrinsic factor + B12 deficiency (associated with other autoimmune)
  • Malabsorption = Crohn’s, coelaic
  • Dietary (vegans)
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60
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
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61
Q

B12/PERNICIOUS ANAEMIA
Investigations for B12/pernicious anaemia?

A
  • FBC (MCV>100fL, low Hb)
  • Serum B12 decreased
  • Blood film = hypersegmented neutrophil nuclei
  • Intrinsic factor Ab for pernicious (gastric parietal cell Ab can be tested by less helpful)
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62
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
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63
Q

AOCD
What are some mechanisms in anaemia of chronic disease (AOCD)?

A
  • Decreased release of iron from bone marrow to developing erythroblasts
  • Inadequate erythropoietin response to anaemia
  • High levels of hepcidin expression (reduces iron transport from duodenal cells to plasma)
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64
Q

AOCD
What are some causes of AOCD?

A
  • Chronic inflammatory diseases = Crohn’s, RA)
  • Chronic infections (TB)
  • Malignancy
  • TB
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65
Q

AOCD
What is the management of AOCD?

A
  • FBC (low Hb)
  • Blood film = normochromic normocytic
  • Low serum iron, transferrin saturation + TIBC
  • High ferritin
  • Treat underlying cause, sometimes recombinant erythropoietin
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66
Q

CLL
What is chronic lymphocytic leukaemia (CLL)?

A
  • Monoclonal proliferation of well differentiated lymphocytes, 99% B cells
  • # 1 leukaemia in adults
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67
Q

CLL
What are some complications of CLL?

A
  • Warm autoimmune haemolysis > anaemia
  • Infection (hypogammaglobulinaemia)
  • Richter’s transformation = high-grade (large B cell) lymphoma
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68
Q

CLL
What is the clinical presentation of CLL

A
  • Incidental finding on FBC
  • Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
  • Weight loss, sweats + anorexia
  • Hepatosplenomegaly, rubbery non-tender lymphadenopathy
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69
Q

CLL
What are some investigations for CLL?

A
  • FBC = pancytopenia
  • Blood film = smudge or smear cells
  • LDH may be raised
  • Bone marrow biopsy is diagnostic
  • CT CAP to stage
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70
Q

CLL
What is the management of CLL?

A
  • No sx = watch + wait
  • Chemo + radio to help lymphadenopathy + splenomegaly
  • Bone marrow transplant
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71
Q

MYELODYSPLASTIC
What is myelodysplastic syndrome?
Risk?

A
  • Immature blood cells in bone marrow do not mature properly + so do not become healthy blood cells
  • Transform to AML
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72
Q

MYELODYSPLASTIC
How might myelodysplastic syndrome present?

A
  • > 60y + previous chemo or radiotherapy
  • ?Incidental finding
  • Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
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73
Q

MYELODYSPLASTIC
Investigations for myelodysplastic syndrome?

A
  • FBC = pancytopenia, reduced reticulocytes
  • Blood film = blasts (ring sideroblasts)
  • Bone marrow aspiration + biopsy = hypercellular bone marrow
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74
Q

MYELODYSPLASTIC
What is the management of myelodysplastic syndrome?

A
  • Watch + wait with supportive Tx = blood transfusions, EPO, G-CSF
  • Chemo or stem cell transplant
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75
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

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76
Q

TYPE 1 DIABETES
what is T1DM?

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.

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77
Q

TYPE 1 DIABETES
what is the pathophysiology of T1DM

A
  • autoimmune destruction of beta cells in the Islets of Langerhans by autoantibodies cause insulin deficiency and continued breakdown of liver glycogen
    this causes hyperglycaemia and glycosuria
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78
Q

TYPE 1 DIABETES
Is T1DM characterised by a problem with insulin secretion, insulin resistance or both?

A

Characterised by impaired insulin secretion - severe insulin deficiency

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79
Q

TYPE 1 DIABETES
what are the risk factors for developing T1DM?

A
  • Northern European
  • Family History:
    - HLA DR3-DQ2 or
    - HLA-DR4-DQ8
  • Other autoimmune diseases:
    - Autoimmune thyroid
    - Coeliac disease
    - Addison’s disease
    - Pernicious anaemia
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80
Q

TYPE 1 DIABETES
what are the clinical features of T1DM?

A

Thirst (fluid and electrolyte losses)
Polyuria (due to osmotic diuresis)
Weight loss

  • usually short history of severe symptoms
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81
Q

TYPE 1 DIABETES
Describe the epidemiology of T1DM

A

Onset younger (<30 years)
Usually lean
More Northern European ancestry

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82
Q

TYPE 1 DIABETES
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?

A

Fasting plasma glucose >7 mmol/L

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83
Q

TYPE 1 DIABETES
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?

A

Random plasma glucose >11 mmol/L

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84
Q

TYPE 1 DIABETES
What might someone’s HbA1c be if they have diabetes?

A

> 48 mmol/L
6.5%

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85
Q

TYPE 1 DIABETES
What happens to C-peptide in T1DM?

A

C-peptide reduces

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86
Q

TYPE 1 DIABETES
How do you treat T1DM?

A

Education
Glycaemic control through diet (low sugar, low fat, high starch)
Insulin SC

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87
Q

TYPE 1 DIABETES
Give 6 complications to Diabetes Mellitus

A
  1. Diabetic ketoacdiosis
  2. Diabetic nephropathy
  3. Diabetic retinopathy
  4. Diabetic neuropathy
  5. Hyperosmolar hyperglycaemic nonteotic coma
  6. Stroke, ischaemic heart disease, peripheral vascular disease
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88
Q

TYPE 1 DIABETES
Give 2 potential consequences of T1DM

A
  1. Hyperglycaemia
  2. Raised plasma ketones –> ketoacidosis
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89
Q

TYPE 1 DIABETES
How is insulin administered in someone with T1DM?

A

Subcutaneous injections

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90
Q

TYPE 1 DIABETES
Other than SC injections, how else can insulin be administered?

A

Insulin pump

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91
Q

TYPE 1 DIABETES
what are the different types of insulin used to treat T1DM?

A
  • short acting - 4-6hrs
  • short acting analogues -
  • long acting - 12-24hrs
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92
Q

TYPE 1 DIABETES
Give 4 potential complications of insulin therapy

A
  1. Hyperglycaemia
  2. Lipohypertrophy at injection site
  3. Insulin resistance
  4. Weight gain
  5. Interference with life style
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93
Q

TYPE 2 DIABETES
Is T2DM characterised by problem with insulin secretion, insulin resistance or both?

A

Characterised by impaired insulin secretion and insulin resistance

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94
Q

TYPE 2 DIABETES
what is the aetiology of T2DM?

A
  • Decreased insulin secretion and increased insulin resistance
  • No immune disturbance
  • No HLA disturbance but strong genetic link
  • Polygenic
  • Associated with obesity, lack of exercise, calorie and alcohol excess
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95
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

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96
Q

TYPE 2 DIABETES
Why is insulin secretion impaired in T2DM

A

Due to lipid deposition in the pancreatic islets

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97
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

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98
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

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99
Q

TYPE 2 DIABETES
Why do you rarely see diabetic ketoacidosis in T2DM?

A

Insulin secretion is impaired but there are still low levels of plasma insulin
Low levels of insulin prevent muscle catabolism and ketogenesis

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100
Q

TYPE 2 DIABETES
By how much has the beta cell mass reduced in T2DM when diagnosis usually occurs?

A

50% of normal beta cell mass

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101
Q

TYPE 2 DIABETES
Describe the epidemiology of T2DM

A

Onset older (>30)
Usually overweight
More common in African/Asian populations
Males > Females

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102
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
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103
Q

TYPE 2 DIABETES
How does metformin work in treating T2DM?

A

Increase insulin sensitivity and inhibits glucose production

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104
Q

TYPE 2 DIABETES
How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

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105
Q

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

A

Hypoglycaemia

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106
Q

REACTIVE ARTHRITIS
What is reactive arthritis?

A

● A sterile synovitis which occurs following
o A GI infection with Shigella, Salmonella, Yersinia or Campylobacter
o Sexually acquired infection
● Typically affects lower limb

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107
Q

REACTIVE ARTHRITIS
What GI infections are associated with causing reactive arthritis?

A

Salmonella
Shigella
Yersinia enterocolitica
campylobacter

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108
Q

REACTIVE ARTHRITIS
What GU infections are associated with causing reactive arthritis?

A

Chlamydia
Ureaplasma urealyticum

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109
Q

REACTIVE ARTHRITIS
What is the classic triad of symptoms for reactive arthritis?

A
  1. Arthritis
  2. Conjunctivitis
  3. Urethritis
    (can’t see, can’t pee, can’t climb a tree)
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110
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)

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111
Q

REACTIVE ARTHRITIS
How is reactive arthritis treated?

A

NSAID
Corticosteroids
DMARD - chronic arthritis

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112
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

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113
Q

FIBROMYALGIA
Name 4 diseases that fibromyalgia is commonly associated with

A
  1. Depression
  2. Choric fatigue
  3. IBS
  4. Chronic headache
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114
Q

FIBROMYALGIA
Give 4 symptoms of fibromyalgia

A
  1. Neck and back pain
  2. Pain is aggravated by stress, cold and activity
  3. Generalised morning stiffness
  4. Paraesthesia of hands and feet
  5. Profound fatigue
  6. Unrefreshing sleep
  7. poor concentration, brain fog
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115
Q

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

A
  1. Hypothyroidism
  2. SLE
  3. Low vitamin D
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116
Q

FIBROMYALIGA
How is fibromyalgia diagnosed?

A

Everything seems normal
11/18 trigger points
Exclude other diagnoses

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117
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)
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118
Q

FIBROMYALGIA
what is the epidemiology of fibromyalgia?

A

women,
poor socioeconomic status,
20-50 year old

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119
Q

FIBROMYALGIA
what is the the pathophysiology of fibromyalgia?

A

Unknown, possibly pain perception/hyper excitability of pain fibres

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120
Q

FIBROMYALGIA
what are the complications of fibromyalgia?

A
  • can really affect quality of life
  • anxiety, depression, insomnia
  • opiate addiction
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121
Q

FIBROMYALGIA
what is fibromyalgia?

A

Also known as chronic persistent pain
● Widespread msk pain after other diseases have been excluded
● Symptoms present at least 3 months and other causes have been excluded

● Characterised by central (non-nociceptive) pain
o Due to a central disturbance in pain processing
o Biopsychosocial factors important
● Not easily diagnosed as there is no specific pathology

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122
Q

GOUT
What is gout?

A

Crystal arthritis
Inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals

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123
Q

GOUT
Describe the epidemiology of gout?

A

● 5x more common in men
● Occurs rarely before young adulthood
● Rarely occurs in pre-menopausal females
● Often a family history

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124
Q

GOUT
What joint does gout most commonly affect?

A

Big toe metatarsophalangeal joint

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125
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

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126
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
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127
Q

GOUT
Name 3 common precipitants of a gout attack

A
  1. Aggressive introduction of hypouricaemic therapy
  2. Alcohol or shellfish binges
  3. Sepsis, MI, acute severe illness
  4. Trauma
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128
Q

GOUT
Name 4 diseases that someone with gout might have an increased risk of developing

A
  1. Hypertension
  2. CV disease - e.g. stroke
  3. Renal disease
  4. Type 2 diabetes
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129
Q

GOUT
what is the clinical presentation of gout?

A

SYMPTOMS
inflamed joints - 1st metatarsal and distal interphalangeal often affected.

SIGNS
tophi- lumps of urate salts

130
Q

GOUT
What are tophi?

A

Onion like aggregates of urate crystals with inflammatory cells. Proteolytic enzymes are released –> erosion

131
Q

GOUT
What investigations might you do in a patient you think has gout?

A

Joint aspiration & polarised light microscopy (needle like negative birefringent crystals),
Increased Urate on blood test
X-ray = rat bite erosions

132
Q

GOUT
What is the aim of treatment for gout?

A

To get urate levels < 300 mol/L

133
Q

GOUT
How would you treat acute gout?

A

Ice packs and rest
NSAIDS
Colchicine = anti-gout medication
Corticosteroids - IM or IA

134
Q

GOUT
Name 3 treatment options for gout

A
  1. Lifestyle modifications - diet, weight loss, reduce alcohol
  2. Allopurinol (xanthine oxidase inhibitor)
  3. NSAIDs or colchicine
    IM prednisolone
135
Q

GOUT
You see a patient with gout who is taking bendroflumethiazide. What drug might you replace this with to help treat their gout?

A

You would switch bendroflumethiazide to cosartan as bendroflumethiazide is a diuretic and so impairs urate excretion

136
Q

GOUT
Name 6 factors that can cause an acute attack of gout

A
  1. Sudden overload
  2. Cold
  3. Trauma
  4. Sepsis
  5. Dehydration
  6. Drugs
137
Q

GOUT
A patient presents with an acute mono-arthropathy of their big toe. What are the two main differential diagnoses?

A
  1. Gout
  2. Septic arthritis
138
Q

GOUT
A patient presents with an acute mono-arthropathy of their big toe. What investigations might you do?

A

Joint aspirate
If septic arthritis - high WCC and neutrophilia and bacteria on gram stain
If gout - urate crystals

139
Q

PSEUDOGOUT
Describe the pathophysiology of pseudogout

A

Calcium pyrophosphate crystals are deposited on joint surfaces - produces the radiological appearance of chondrocalcinosis
Crystals elicit an acute inflammatory response

140
Q

PSEUDOGOUT
What can cause pseudogout?

A
  1. Hypo/hyperthyroidism
  2. Haemochromatosis
  3. Diabetes
  4. Magnesium levels
141
Q

PSEUDOGOUT
what is the clinical presentation of pseudogout?

A

SYMPTOMS
hot, swollen, tender joint, usually knees

SIGNS
recent injury to the joint in the history

Typically the wrists and knees

142
Q

PSEUDOGOUT
What investigations might you do in someone you suspect might have pseudogout?

A

Aspiration –> fluid for crystals and blood cultures = positive birefringent rhomboid crystals

X-rays –> can show chondrocalcinosis

143
Q

PSEUDOGOUT
What is the most likely differential diagnosis for pseudogout?

144
Q

PSEUDOGOUT
Describe the treatment for pseudogout

A
  • high dose NSAIDs - ibuprofen
  • Colchicine - anti-gout
  • IM prednisolone
  • Aspiration, intra-articular steroid injections
145
Q

PSEUDOGOUT
What kind of crystals do you see in pseudogout?

A

Positive birefringent calcium pyrophosphate rhomboid crystals

146
Q

GOUT
What kind of crystals do you see in gout?

A

Monosodium urate crystals = negatively birefringent

147
Q

PSEUDOGOUT
What kind of crystals fo you see in pseudogout?

A

Calcium pyrophosphate crystals = positively birefringent

148
Q

BPH
What is benign prostatic hypertrophy (BPH)?
Complications?

A
  • Overgrowth of prostatic tissue in transitional (inner) zone which compresses prostatic urethra
  • Obstruction not relieved may get infection (stasis) or hydroureter/nephrosis
149
Q

BPH
How does BPH present?

A

LUTS:
- Storage Sx (FUN) = Frequency, Urgency, Nocturia
- Voiding Sx (HIT) = Hesitancy, Intermittent flow, Terminal dribbling
UTI secondary to stasis, acute or chronic retention

150
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
151
Q

BPH
What is the conservative management of BPH?

A
  • Avoid caffeine + alcohol
  • Relax when voiding + void twice in a row to aid emptying
  • Control urgency with distraction methods
152
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
153
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

154
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)
155
Q

HAEMATURIA
What can cause…

i) transient or non-visible haematuria?
ii) persistent non-visible haematuria?
iii) other?

A

i) UTI, menstruation, vigorous exercise (normally settles after 3d), sex
ii) Cancer (TCC, RCC, prostate), stones, BPH, prostatitis, urethritis
iii) Red/orange urine but no haematuria = beetroot, rifampicin

156
Q

HAEMATURIA
What investigations might you do for haematuria?

A
  • Urine dipstick initially (persistent = present in 2/3 samples 2w apart)
  • Check renal function, ACR or PCR + BP
157
Q

HAEMATURIA
What would warrant an urgent referral regarding haematuria?

A
  • ≥45 + unexplained visible haematuria or persists after successful UTI Mx
  • ≥60 + unexplained non-visible haematuria + dysuria or raised WCC
  • Non-urgent if ≥60 + recurrent or persistent unexplained UTI
158
Q

CKD
Define chronic kidney disease

A

Long standing, usually progressive, impairment in renal function for more than 3 months

159
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)
160
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)

161
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
162
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)
163
Q

CKD
What investigations might be done in someone who has CKD?

A

FBC = anaemia
U+Es = raised phosphate, uric acid, urea, creatine and decreased Calcium
Urine dipstick = haematuria and proteinuria
GFR
Imaging - USS, CT KUB, ECG, Xrays

164
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

165
Q

PROSTATE CANCER
Define prostate cancer

A

Adenocarcinoma in the peripheral zone of the prostate gland

166
Q

PROSTATE CANCER
Where can prostate cancer metastasise to?

A

Lymph nodes and bone

Rarely = brain, liver, lung

167
Q

PROSTATE CANCER
By what routes can prostate cancer spread?

A
  1. Lymphatic - to external iliac and internal iliac and presacral node
  2. Haematogenous - to bone, lung. liver, kidneys
  3. Direct - within in the prostate capsule
168
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

169
Q

PROSTATE CANCER
what are the symptoms of prostate cancer?

A
  1. LUTS
  2. Bone pain, weight loss, night sweats
    anaemia = mets
    Most picked up in asymptomatic stage
170
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

171
Q

PROSTATE CANCER
What grading system is used in prostate cancer?

A

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

172
Q

PROSTATE CANCER
What is the treatment for localised prostate cancer?

A

prostatectomy (<70),
active surveillance (>70 and low risk),
radiotherapy

173
Q

PROSTATE CANCER
What is the treatment for metastatic prostate cancer?

A
  • chemotherapy,
  • radiotherapy,
  • bilateral orchidectomy (gold standard hormonal treatment),
  • Goserelin (LHRH receptor blocker),
  • palliative treatments focus on relieving symptoms e.g. TURP
174
Q

PROSTATE CANCER
Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer

A

Advantages:
1. Curative
2. Reduced patient anxiety
Disadvantages:
1. Can have adverse effects

175
Q

PROSTATE CANCER
How do LH antagonists work in treating prostate cancer?

A

First stimulate and then inhibit pituitary gonadotrophin
E.g. Leuprolide

176
Q

PROSTATE CANCER
Is a raised PSA confirmatory of prostate cancer?

A

NO
Prostate cancer indication

177
Q

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

A
  1. Benign prostate enlargement
  2. UTI
  3. Prostatitis
178
Q

PROSTATE CANCER
Give 2 advantages and 2 disadvantages of screening in prostate cancer

A

Advantages:
1. Early diagnosis of localised disease (cure)
2. Early treatment of advanced disease (effective palliation)
Disadvantages:
1. Over diagnosis of insignificant disease
2. Harm caused by investigation/treatment

179
Q

PROSTSTE CANCER
What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream

180
Q

UTI
Define urinary tract infection

A

Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria

181
Q

UTI
What determines if a UTI is complicated or uncomplicated?

A

A UTI is deemed complicated if it affects:

  • Someone with an abnormal urinary tract
  • A man
  • Pregnant lady
  • Children
  • Immunocompromised
  • If it is recurrent
182
Q

UTI
Describe the pathophysiology of UTI’s

A

Organisms colonise the urethral meatus –> bacterial sent –> bacteriuria

183
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
184
Q

UTI
Describe the epidemiology of UTI’s

A

More common in women due to short urethra and its proximity to the anus

185
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
186
Q

UTI
Give 3 bacterial virulence factors that aid their ability to cause UTI’s

A
  1. Fimbriae/pili that adhere to urothelium
  2. Acid polysaccharide coat resists phagocytes
  3. Toxins (e.g. UPEC releases cytotoxins)
  4. Enzyme production (e.g. urease)
187
Q

UTI
What type of pili would you associate with lower UTI?

A

Type 1
Bind to uroplakin

188
Q

UTI
What type of pili would you associate with upper UTI?

A

Type P
Bind to glycolipids on urothelium

189
Q

UTI
The vagina is heavily colonised with lactobacilli, what is the function of this?

A

Helps maintain a low pH = host defence mechanism

190
Q

UTI
Give 2 reasons why a post-menopausal women is more susceptible to a UTI

A
  1. pH rises –> increased colonisation by colonic flora
  2. Reduced mucus secretion
191
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
192
Q

UTI
Define pyuria

A

Presence of pus in urine

193
Q

UTI
Name 4 lower urinary tract infections

A
  1. Cystitis
  2. Prostatitis
  3. Epididymo-orchitis
  4. Urethritis
194
Q

UTI
Name a upper urinary tract infection

A

Pyelonephritis

195
Q

UTI
Give 4 classic UTI symptoms

A
  1. Urgency
  2. Frequency
  3. Dysuria
  4. Haematuria
  5. Abdominal pain
  6. Malaise
  7. Confusion (old patients)
196
Q

UTI
What investigations might you do in someone who you suspect has a UTI?

A
  1. Take a good history
  2. Urinalysis –> haematuria, proteinuria, increased WCC, pH, nitrates, ketones
  3. Microscopy, culture and sensitivity of MSU
    4 In recurrent/complicated UTI = imaging (bladder scan, USS, XR)
197
Q

UTI
What is the first line treatment for an uncomplicated UTI?

A

Trimethoprim or nitrofurantoin for 3 days

Increase fluid intake and regular voiding

198
Q

UTI
How does trimethoprim work?

A

It affects folic acid metabolism

199
Q

UTI
Describe the management for a complicated UTI

A

Culture sample –> Abx for 7 days

200
Q

UTI
Define recurrent UTI

A

> 2 episodes in 6 months or >3 in 12 months

201
Q

UTI
Describe the management for someone who is having recurrent UTIs

A
  1. Increase fluid intake
  2. Regular voiding
  3. Void pre and post intercourse
  4. Abx prophylaxis
  5. Vaginal oestrogen replacement
202
Q

ACNE VULGARIS
what is it?

A

Acne vulgaris is a common skin disorder which usually occurs in adolescence. It typically affects the face, neck and upper trunk and is characterised by the obstruction of the pilosebaceous follicle with keratin plugs which results in comedones, inflammation and pustules.

203
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
204
Q

ACNE VULGARIS
what is the clinical presentation of mild acne?

A

open and closed comedones with or without sparse inflammatory lesions

205
Q

ACNE VULGARIS
what is the clinical presentation of moderate acne?

A

widespread non-inflammatory lesions and numerous papules and pustules

206
Q

ACNE VULGARIS
what is the clinical presentation of severe acne?

A

extensive inflammatory lesions, which may include nodules, pitting, and scarring

207
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

208
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

209
Q

IMPETIGO
what is impetigo and what is it caused by?

A

it is a superficial bacterial skin infection
caused by staph. aureus or strep. pyogenes

210
Q

IMPETIGO
where does it affect on the body?

A

anywhere but lesions tend to occur on face, flexures and limbs not covered by clothing

211
Q

IMPETIGO
how is impetigo spread?

A

Spread is by direct contact with discharges from the scabs of an infected person.

The bacteria invade the skin through minor abrasions and then spread to other sites by scratching.

Infection is spread mainly by the hands, but indirect spread via toys, clothing, equipment and the environment may occur.

212
Q

IMPETIGO
what is the incubation time?

A

between 4 to 10 days.

213
Q

IMPETIGO
what are the clinical features?

A

‘golden’, crusted skin lesions typically found around the mouth
very contagious

214
Q

IMPETIGO
what is the management?

A
  • 1% hydrogen peroxide (in all who are not systemically unwell or at high risk of complications)
  • topical abx creams - topical fusidic acid, topical mupirocin if resistant or MRSA
  • extensive disrease = oral flucloxacillin or erythromycin
215
Q

IMPETIGO
hoe long should a child be excluded from school?

A
  • until lesions are crusted and healed or 48 hours after commencing antibiotic treatment
216
Q

GLANDULAR FEVER
what causes it?

A

EBV (also known as HHV-4) - most cases
CMV
HHV-6

217
Q

GLANDULAR FEVER
what is the classic triad of symptoms?

A
  • sore throat
  • lymphadenopathy: may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged
  • pyrexia
218
Q

GLANDULAR FEVER
what are the other symptoms?

A

malaise, anorexia, headache
palatal petechiae
splenomegaly
hepatitis, transient rise in ALT
lymphocytosis
haemolytic anaemia secondary to cold agglutins (IgM)
a maculopapular, pruritic rash

219
Q

GLANDULAR FEVER
how long does it typically take for symptoms to resolve?

220
Q

GLANDULAR FEVER
what are the investigations?

A

heterophil antibody test (Monospot test)
NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.

221
Q

GLANDULAR FEVER
what is the management?

A

rest during the early stages, drink plenty of fluid, avoid alcohol
simple analgesia for any aches or pains
avoid playing contact sports for 4 weeks after having glandular fever to reduce the risk of splenic rupture

222
Q

LYME DISEASE
what is lyme disease caused by?

A

spirochaete Borrelia burgdorferi and is spread by tick

223
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
224
Q

LYME DISEASE
what are the later features of lyme disease?

A

CVS
- heart block
- peri/myocarditis

neurological
- facial nerve palsy
- radicular pain
- meningitis

225
Q

LYME DISEASE
what are the investigations?

A
  • diagnosed clinically if erythema migrans is present
  • ELISA test
  • immunoblot for lyme disease
226
Q

LYME DISEASE
what is the management of asymptomatic tick bites?

A
  • if tick is still present, remove using fine tipped tweezers
227
Q

LYME DISEASE
what is the management?

A
  • doxycycline (amoxicillin if pregnant)
  • ceftriaxone in disseminated disease
228
Q

MEASLES
what is it caused by?

A

RNA paramyxovirus

229
Q

MEASLES
how is it spread and what is the incubation period?

A
  • aerosol transmission
  • 10-14 days
230
Q

MEASLES
when are you infectious with measles?

A

from prodrome to 4 days after the rash starts

231
Q

MEASLES
what are the clinical features?

A
  • prodrome = irritable, conjunctivitis, fever
  • Koplik spots (white spots on buccal mucosa)
  • rash ( starts behind ear + spreads to entire body, maculopapular rash, desquamation spares palms and soles)
  • diarrhoea
232
Q

MEASLES
what are the investigations?

A
  • IgM antibodies
233
Q

MEASLES
what is the management?

A

mainly supportive
admission may be considered in immunosuppressed or pregnant patients
notifiable disease → inform public health

234
Q

MEASLES
what are the complications?

A
  • otitis media = most common
  • pneumonia = most common cause of death
  • encephalitis
  • subacute sclerosing panencephalitis
  • febrile convulsions
  • keratoconjunctivitis
  • diarrhoea
235
Q

MEASLES
what is the management for contacts?

A
  • if child is not immunised, MMR vaccine should be offered within 72 hours
236
Q

MUMPS
what is mumps caused by?

A

RNA paramyxovirus

237
Q

MUMPS
how is it spread and what is the incubation period?

A
  • spread by droplets
  • incubation = 14-21 days
238
Q

MUMPS
when are you infectious?

A

7 days before and 9 days after parotid swelling starts

239
Q

MUMPS
what is the clinical presentation?

A

fever
malaise, muscular pain
parotitis (‘earache’, ‘pain on eating’): unilateral initially then becomes bilateral in 70%
parotid gland swelling

240
Q

MUMPS
what is the management?

A

rest
paracetamol for high fever/discomfort
notifiable disease

241
Q

MUMPS
what are the complications?

A
  • orchitis
  • hearing loss - usually unilateral and transient
  • meningoencephalitis
  • pancreatitis
242
Q

URTICARIA
what is it?

A

Urticaria describes a local or generalised superficial swelling of the skin. The most common cause of urticaria is allergy although non-allergic causes are seen.

243
Q

URTICARIA
what are the clinical features?

A

pale, pink raised skin. Variously described as ‘hives’, ‘wheals’, ‘nettle rash’
pruritic

244
Q

URTICARIA
what is the management?

A

non-sedating antihistamines are first-line
prednisolone is used for severe or resistant episodes

245
Q

ANAPHYLAXIS
what is it defined as?

A

Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction.

246
Q

ANAPHYLAXIS
what are the clinical features?

A

the sudden onset and rapid progression of symptoms

Airway - swelling of the throat and tongue →hoarse voice and stridor

Breathing problems -
respiratory wheeze, dyspnoea

Circulation problems -
hypotension, tachycardia

Skin changes - generalised pruritis, erythematous or urticarial rash

247
Q

ANAPHYLAXIS
what are the most common causes?

A

food (e.g. nuts) - the most common cause in children
drugs
venom (e.g. wasp sting)

248
Q

ANAPHYLAXIS
what is the emergency management?

A

500 micrograms IM adrenaline every 5 minutes

IV fluid bolus

249
Q

ANAPHYLAXIS
what is refractory anaphylaxis?

A

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

250
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

251
Q

ANAPHYLAXIS
what is the management following initial stabilisation?

A
  • non-sedating antihistamines
  • take serum tryptase levels
  • referral to allergy clinic
  • give 2x adrenaline injectors + training
252
Q

CONJUNCTIVITIS
what are the different types?

A

It is commonly split into three categories:

allergic
viral
bacterial

253
Q

CONJUNCTIVITIS
what are the general clinical features?

A
  • red, painful eye that may feel gritty/itchy
  • discharge
  • photophobia (suggests corneal involvement)
  • visual acuity should not be affected
254
Q

CONJUNCTIVITIS
what are the clinical features of allergic conjunctivitis?

A
  • serous discharge from eyes
  • conjunctival oedema in severe cases
  • symptoms are exacerbated at certain times of the year
255
Q

CONJUNCTIVITIS
what is the cause of allergic conjunctivitis?

A

type 1 hypersensitivity reaction due to airborne allergens

256
Q

CONJUNCTIVITIS
what is the management of allergic conjunctivitis?

A

conservative management
avoid allergen
artificial tears (dilutes allergen)
antihistamines

257
Q

CONJUNCTIVITIS
what are the clinical features of viral conjunctivitis?

A
  • serous discharge
  • more likely to be unilateral
  • more common than bacterial
258
Q

CONJUNCTIVITIS
what is the management of viral conjunctivitis?

A

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

259
Q

CONJUNCTIVITIS
what are the clinical features of bacterial conjunctivitis?

A
  • purulent discharge
  • eyelids stuck together
260
Q

CONUNCTIVITIS
what are the causes of bacterial conjunctivitis?

A
  • staph. epidermis
  • staph. aureus
  • strep. pneumoniae
  • H. influenzae
  • chlamydia
  • gonorrhoea
261
Q

CONJUNCTIVITIS
what is the management of bacterial conjunctivitis?

A
  • resolves within 7-14 days
  • topical chloramphenicol
  • lubricating eye drops
262
Q

INFLUENZA
what are the different types of flu?

A

A, B and C
different host organisms produce different strains

263
Q

INFLUENZA
what type of virus is flu?

A

RNA single stranded virus

264
Q

INFLUENZA
how is it transmitted?

A

via respiratory droplets

265
Q

INFLUENZA
what are the clinical features?

A

Fever ≥ 37.8°C
Non-productive cough
Myalgia
Headache
Malaise
Sore throat
Rhinitis

266
Q

INFLUENZA
what is the incubation period and infectious period for influenza?

A

incubation period = 1-4 days

infectious period = 7-21 days

267
Q

INFLUENZA
what are the complications?

A

Pulmonary: Viral pneumonia, secondary bacterial pneumonia, worsening of chronic conditions e.g. COPD and asthma

Cardiovascular: Myocarditis, heart failure

Neurological: Encephalopathy

Gastrointestinal: Anorexia and vomiting are common

268
Q

INFLUENZA
how is it diagnosed?

A

PCR testing

269
Q

INFLUENZA
what is the management?

A

Largely supportive (analgesia, antipyretic, fluids, oxygen)

Antiviral treatment with neuraminidase inhibitors e.g. Oseltamivir (‘Tamiflu’)

Infection control and respiratory isolation to prevent onward transmission

270
Q

INFLUENZA
how can it be prevented?

A

vaccination - inactivated vaccine

recommended for over 65, chronic condition, healthcare workers, nursing home residents

271
Q

BURSITIS
what is it?

A

A painful condition where bursae of joints become inflamed

272
Q

BURSITIS
what are the most common locations?

A

shoulder
elbow
hip
Often occurs near joints that experience repetitive movements

273
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

274
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

275
Q

BURSITIS
what are the risk factors?

A
  • age
  • occupation
  • systemic conditions such as RA, gout and DM
  • obesity
276
Q

BURSITIS
how can it be prevented?

A
  • use kneeling pads
  • lift properly
  • take frequent breaks
  • weight loss
  • exercising
277
Q

BURSITIS
what are the investigations?

A
  • clinical diagnosis
  • x-ray
  • USS or MRI
  • FBC with CRP, ESR
278
Q

BURSITIS
what is the management?

A
  • anti-inflammatory - NSAIDs
  • antibiotics for infection
  • physiotherapy
  • corticosteroid injections
  • crutches to relieve pressure
  • surgical drainage
279
Q

CONTACT DERMATITIS
What is it?

A

type of eczema triggered by contact with a particular substance

It usually improves/clears up if the substance causing the problem is avoided

280
Q

CONTACT DERMATITIS
what are the symptoms?

A

skin becomes itchy, blistered, dry and cracked
light skin = red
darker skin = purple or grey

usually occurs on hands and face within few hours/days of exposure

281
Q

CONTACT DERMATITIS?
what are the causes?

A
  • irritants - frequent exposure to weak irritants e.g. soaps, antiseptics, perfumes etc
  • allergens - becomes sensitised with first exposure but no reactions. Subsequent exposures result in reactions e,g, cosmetics, nickel/cobalt jewellery, rubber
282
Q

CONTACT DERMATITIS
what are the investigations?

A
  • clinical diagnosis
  • identification of irritants/allergens through history or patch testing
283
Q

CONTACT DERMATITIS
what is the management?

A
  • avoid the cause
  • emollients
  • topical corticosteroids
  • steroid tablets if severe
284
Q

CUTANEOUS WARTS
what are the causes?

A

HPV infection
This causes an excess amount of keratin to develop in the epidermis

285
Q

CUTANEOUS WARTS
are they contagious?

A
  • They aren’t considered very contagious by can be caught be close skin-to-skin contact
  • infection can also be caught indirectly from contaminated objects or surfaces e.g. swimming pool
286
Q

CUTANEOUS WARTS
what are the symptoms?

A
  • not usually painful
  • occasionally itch/bleed
287
Q

CUTANEOUS WARTS?
what are the different types?

A
  • common warts (verruca vulgaris) - on knuckles, fingers and knees
  • verrucas (plantar warts) - on soles of feet
  • mosaic warts - clusters on palms of hands and soles of feet
  • periungal warts - under and around finger/toenails
  • filiform warts - long + slender, on face + neck
  • plane warts
288
Q

CUTANEOUS WARTS
what is the management?

A
  • will usually clear without treatment but can take up to 2 years to clear system
  • salicylic acid
  • cryotherapy
  • chemical treatment - formaldehyde, silver nitrate
289
Q

CUTANEOUS WARTS
how can they be prevented?

A
  • keep feet dry
  • change socks everyday
  • wear pool slippers/flip flops
  • cover wart to prevent spread to other people
290
Q

FOLLICULITIS
what is it?

A

common condition where hair follicles become inflamed

291
Q

FOLLICULITIS
what are the symptoms?

A
  • clusters of small bumps/pimples around hair follicles
  • pus-filled blisters that break open and crust over
  • itchy, burning skin
  • painful, tender skin
  • an inflamed bump
292
Q

FOLLICULITIS
what are the 2 main types?

A
  • superficial - involves part of the follicle
  • deep - involves the entire follicle and is usually more severe
293
Q

FOLLICULITIS
what are the causes?

A
  • staph aureus infection

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

294
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
295
Q

FOLLICULITIS
how can it be prevented?

A
  • wash skin regularly
  • do laundry regularly
  • avoid friciton/pressure on skin
  • avoid shaving
296
Q

FOLLICULITIS
what is the management?

A
  • antibiotic lotion
  • antifungal shampoos
  • creams to calm inflammation
297
Q

BENIGN EYELID DISORDERS - BLEPHARITIS
what is it?

A
  • inflammation of the eyelid
298
Q

BENIGN EYELID DISORDERS - BLEPHARITIS
what are the symptoms?

A
  • bilateral symptoms
  • ocular irritation
  • foreign body sensation
  • burning
  • redness
  • crusting
299
Q

BENIGN EYELID DISORDERS - BLEPHARITIS
what is the pathophysiology?

A

congestion and inflammation of eyelash follicles + meibomian glands

300
Q

BENIGN EYELID DISORDERS - BLEPHARITIS
what are the causes?

A

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

301
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

302
Q

BENIGN EYELID DISORDERS - STYE
what is it?

A

infection of eyelash follicle
also known as hordeolum

303
Q

BENIGN EYELID DISORDERS - STYE
what is the cause?

A

staph infection of eyelash follicle

304
Q

BENIGN EYELID DISORDERS - STYE
what are the symptoms?

A

tender red eyelash follicle swellings

305
Q

BENIGN EYELID DISORDERS - STYE
what is the management?

A

most self resolve
- warm compression
- removal of eyelash
- incision with sterile needle
- topical antibiotics (chloramphenicol) or co-amoxiclav PO if recurrent or severe

306
Q

BENIGN EYELID DISORDERS - CHALAZION
what is it?

A

granulomatous inflammation of an obstructed meibomian gland on internal eyelid

307
Q

BENIGN EYELID DISORDERS - CHALAZION
what are the causes?

A
  • non-infectious
  • associated with blepharitis and acne rosacea
308
Q

BENIGN EYELID DISORDERS - CHALAZION
what are the symptoms?

A

painless red eyelid cysts in internal eyelid
non-tender

309
Q

BENIGN EYELID DISORDERS - CHALAZION
what is the management?

A

often resolve spontaneously
- warm compression + eyelid massage

310
Q

BENIGN EYELID DISORDERS - ENTROPION
what is it?

A

inward turning of eyelid

311
Q

BENIGN EYELID DISORDERS - ENTROPION
what are the causes?

A
  • age-related degenerative changes
  • trachoma infection (chlamydia infection of eye)
312
Q

BENIGN EYELID DISORDERS - ENTROPION
what is the management?

A
  • examination for corneal abrasions + ulcers
  • lubricants to reduce risk of abrasions/ulcers
313
Q

BENIGN EYELID DISORDERS - ECTROPION
what is it?

A

outward turning of the eyelid

314
Q

BENIGN EYELID DISORDERS - ECTROPION
what are the causes?

A
  • age-related degenerative changes
  • facial nerve palsy (bell’s palsy)
315
Q

BENIGN EYELID DISORDERS - ECTROPION
what is the clinical presentation?

A

sore red eye
watery due to disrupted tear drainage

316
Q

BENIGN EYELID DISORDERS - ECTROPION
what is the management?

A
  • eye lubrication drops
  • taping eyes shut at night
  • severe = surgery
317
Q

BENIGN EYELID DISORDERS - ECTROPION
what can this condition lead to?

A

exposure keratopathy - can cause sight loss

318
Q

BENIGN EYELID DISORDERS - TRICHIASIS
what is it?

A

when eyelashes grow inwards due to damaged eyelash follicles

319
Q

BENIGN EYELID DISORDERS - TRICHIASIS
what is the most common cause?

A

chronic blepharitis

320
Q

BENIGN EYELID DISORDERS - TRICHIASIS
whay is the management?

A
  • epilating eyelashes (however they reoccur every few weeks)
  • electrolysis/laser ablation can destroy follicle

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