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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
HYPERTHYROIDISM What is the management of hyperthyroidism?
- Beta-blockers for rapid sympathetic control (propranolol) - Carbimazole 1st line, propylthiouracil 2nd - Radioiodine therapy - Surgical thyroidectomy - NSAIDs + beta-blockers for self-limiting DeQuervain's
26
HYPERTHYROIDISM What are the 2 methods for administering anti-thyroid drugs? What are side effects of them?
- Titration - Block + replace (block all production + take levothyroxine) - Carbimazole = agranulocytosis - Propylthiouracil = severe hepatic reactions
27
HYPERTHYROIDISM What are some risks with... i) radioiodine therapy? ii) surgical thyroidectomy?
i) C/I in pregnancy, breastfeeding + may leave patient hypothyroid ii) Risk to recurrent laryngeal nerve (hoarse voice) + hypoparathyroidism
28
HYPOTHYROIDISM What are some common causes of hypothyroidism?
- 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)
29
HYPOTHYROIDISM What is... i) atrophic thyroiditis? ii) Hashimoto's thyroiditis?
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
30
HYPOTHYROIDISM What are some symptoms of hypothyroidism?
- Weight gain, decreased appetite + constipation - Cold intolerance - Lethargy, menorrhagia
31
HYPOTHYROIDISM What are some signs of hypothyroidism?
BRADYCARDIC - Bradycardia - Reflexes relax slowly - Ataxia - Dry, thin hair/skin - Yawning - Cold hands - Ascites - Round puffy face - Defeated demeanour - Immobile - CHF
32
HYPOTHYROIDISM What are some investigations for hypothyroidism?
- 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
33
HYPOTHYROIDISM What is the management of hypothyroidism? Prescribing information?
- Lifelong levothyroxine to replace (titrate up) - 30m before breakfast as iron decreases absorption of thyroxine - Repeat TFTs monthly until stable
34
GALLSTONES What is the clinical presentation of gallstones?
- Severe RUQ may radiate to tip of scapula - N+V - May be triggered by heavy, fatty meal
35
OSTEOARTHRITIS What is osteoarthritis?
- 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)
36
OSTEOARTHRITIS What causes osteoarthritis? Risk factors?
- Secondary OA can occur in joints due to congenital disease + damage - Obesity, increasing age, trauma, female, FHx, occupation (manual labour)
37
OSTEOARTHRITIS What are the main symptoms of osteoarthritis?
- Morning stiffness <30m - Stiffness after rest (gelling) - Bony swellings/joint deformities - Reduced ROM, weak grip + reduced functioning
38
OSTEOARTHRITIS What bony swellings may be seen in osteoarthritis?
- 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)
39
OSTEOARTHRITIS What joints may be affected in osteoarthritis?
- Hips, knees, sacroiliac joints, MCP joint at base of thumb (squaring), wrist, cervical spine
40
OSTEOARTHRITIS What would plain radiograph show in osteoarthritis?
LOSS – - Loss of joint space - Osteophytes - Subarticular sclerosis (increased density of bone along joint line) - Subchondral cysts (fluid filled holes in the bone)
41
OSTEOARTHRITIS What is the conservative management of osteoarthritis?
- Education - Lifestyle (weight loss) - Physio to improve strength - Orthotics to support activities + function (walking aids)
42
OSTEOARTHRITIS What medical treatment may be given for osteoarthritis?
- Regular PO + topical NSAIDs - PO NSAIDs (?+PPI) for intermittent use - ?Opiates like codeine + morphine - Intra-articular steroid injections to reduce inflammation
43
OSTEOARTHRITIS What surgery may be offered in osteoarthritis?
- Arthroscopy for loose bodies (can cause locking e.g. knee) - Osteotomy (changing bone length) - Arthroplasty (joint replacement, risk of infection) - Fusion (often ankle + foot)
44
GOUT What is gout? Pathophysiology?
- Inflammatory arthritis due to hyperuricaemia + intra-articular monosodium urate crystals - Urate derived from breakdown of purines (adenine + guanine)
45
GOUT What are some causes of gout? Who is it most common in?
- Increased uric acid production = chemo, pyrazinamide - Decreased uric acid excretion = diuretics, renal impairment, alcohol excess - Older men
46
GOUT What are some risk factors for gout? What are some factors that may precipitate an attack?
- Alcohol, high purine diet (red meat + seafood), cell damage + Death (surgery, chemo) - Dietary excess, diuretics, dehydration, sepsis
47
GOUT How does gout present?
- Acute hot, swollen + painful joints (exclude septic) - Wrists, base of thumb (carpometacarpal joint) + metatarsophalangeal joint of big toe
48
GOUT What are some signs of gout?
- 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
49
GOUT What investigations would you do for gout?
- 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
50
GOUT What is the management for gout for... i) an acute flare? ii) long-term prophylaxis?
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)
51
PSEUDOGOUT What is pseudogout? What is it associated with?
- Microcrystal synovitis due to deposits of calcium pyrophosphate crystals - Hyperparathyroid, hypothyroid, haemochromatosis, hypophosphataemia
52
PSEUDOGOUT How does pseudogout present?
- Acute hot, swollen + stiff joints - Monoarthropathy affecting shoulders, wrists + knees
53
PSEUDOGOUT What are the investigations for pseudogout?
- 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
54
PSEUDOGOUT What is the management of pseudogout?
- NSAIDs, colchicine - Intra-articular steroids or PO - Joint aspiration of arthrocentesis if severe
55
PMR What is polymyalgia rheumatica (PMR)? Associations?
- Inflammatory condition (vasculitis) causing pain + stiffness in shoulder, pelvic girdle + neck - GCA
56
PMR What is the clinical presentation of PMR
- 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
57
PMR What is the management of PMR?
- ESR/CRP raised, CK normal - PO prednisolone shows dramatic response (diagnostic)
58
B12/PERNICIOUS ANAEMIA What is the pathophysiology of B12 deficiency?
- Absorption of B12 in terminal ileum + intrinsic factor (via gastric parietal cells) dependent for transport across intestinal mucosa
59
B12/PERNICIOUS ANAEMIA What are some causes of B12 deficiecny?
- 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)
60
B12/PERNICIOUS ANAEMIA What are the B12 specific features of the anaemia?
- Peripheral neuropathy with numbness or paraesthesia - Loss of vibration sense or proprioception - Visual, mood or cognitive changes - Glossitis = beefy-red sore tongue
61
B12/PERNICIOUS ANAEMIA Investigations for B12/pernicious anaemia?
- 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)
62
B12/PERNICIOUS ANAEMIA What is the management of B12/pernicious anaemia?
- 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
63
AOCD What are some mechanisms in anaemia of chronic disease (AOCD)?
- 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)
64
AOCD What are some causes of AOCD?
- Chronic inflammatory diseases = Crohn's, RA) - Chronic infections (TB) - Malignancy - TB
65
AOCD What is the management of AOCD?
- FBC (low Hb) - Blood film = normochromic normocytic - Low serum iron, transferrin saturation + TIBC - High ferritin - Treat underlying cause, sometimes recombinant erythropoietin
66
CLL What is chronic lymphocytic leukaemia (CLL)?
- Monoclonal proliferation of well differentiated lymphocytes, 99% B cells - #1 leukaemia in adults
67
CLL What are some complications of CLL?
- Warm autoimmune haemolysis > anaemia - Infection (hypogammaglobulinaemia) - Richter's transformation = high-grade (large B cell) lymphoma
68
CLL What is the clinical presentation of CLL
- 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
69
CLL What are some investigations for CLL?
- FBC = pancytopenia - Blood film = smudge or smear cells - LDH may be raised - Bone marrow biopsy is diagnostic - CT CAP to stage
70
CLL What is the management of CLL?
- No sx = watch + wait - Chemo + radio to help lymphadenopathy + splenomegaly - Bone marrow transplant
71
MYELODYSPLASTIC What is myelodysplastic syndrome? Risk?
- Immature blood cells in bone marrow do not mature properly + so do not become healthy blood cells - Transform to AML
72
MYELODYSPLASTIC How might myelodysplastic syndrome present?
- >60y + previous chemo or radiotherapy - ?Incidental finding - Signs of bone marrow failure – low Hb = anaemia, low WCC = infections, thrombocytopenia = bruising
73
MYELODYSPLASTIC Investigations for myelodysplastic syndrome?
- FBC = pancytopenia, reduced reticulocytes - Blood film = blasts (ring sideroblasts) - Bone marrow aspiration + biopsy = hypercellular bone marrow
74
MYELODYSPLASTIC What is the management of myelodysplastic syndrome?
- Watch + wait with supportive Tx = blood transfusions, EPO, G-CSF - Chemo or stem cell transplant
75
ARRHYTHMIAS Give 3 effects hyperkalaemia on an ECG
GO - absent P wave GO TALL - tall T wave GO long - prolonged PR GO wide - wide QRS
76
TYPE 1 DIABETES what is T1DM?
Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.
77
TYPE 1 DIABETES what is the pathophysiology of T1DM
- 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
78
TYPE 1 DIABETES Is T1DM characterised by a problem with insulin secretion, insulin resistance or both?
Characterised by impaired insulin secretion - severe insulin deficiency
79
TYPE 1 DIABETES what are the risk factors for developing T1DM?
- Northern European - Family History: - HLA DR3-DQ2 or - HLA-DR4-DQ8 - Other autoimmune diseases: - Autoimmune thyroid - Coeliac disease - Addison’s disease - Pernicious anaemia
80
TYPE 1 DIABETES what are the clinical features of T1DM?
Thirst (fluid and electrolyte losses) Polyuria (due to osmotic diuresis) Weight loss - usually short history of severe symptoms
81
TYPE 1 DIABETES Describe the epidemiology of T1DM
Onset younger (<30 years) Usually lean More Northern European ancestry
82
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?
Fasting plasma glucose >7 mmol/L
83
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?
Random plasma glucose >11 mmol/L
84
TYPE 1 DIABETES What might someone's HbA1c be if they have diabetes?
>48 mmol/L >6.5%
85
TYPE 1 DIABETES What happens to C-peptide in T1DM?
C-peptide reduces
86
TYPE 1 DIABETES How do you treat T1DM?
Education Glycaemic control through diet (low sugar, low fat, high starch) Insulin SC
87
TYPE 1 DIABETES Give 6 complications to Diabetes Mellitus
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
88
TYPE 1 DIABETES Give 2 potential consequences of T1DM
1. Hyperglycaemia 2. Raised plasma ketones --> ketoacidosis
89
TYPE 1 DIABETES How is insulin administered in someone with T1DM?
Subcutaneous injections
90
TYPE 1 DIABETES Other than SC injections, how else can insulin be administered?
Insulin pump
91
TYPE 1 DIABETES what are the different types of insulin used to treat T1DM?
- short acting - 4-6hrs - short acting analogues - - long acting - 12-24hrs
92
TYPE 1 DIABETES Give 4 potential complications of insulin therapy
1. Hyperglycaemia 2. Lipohypertrophy at injection site 3. Insulin resistance 4. Weight gain 5. Interference with life style
93
TYPE 2 DIABETES Is T2DM characterised by problem with insulin secretion, insulin resistance or both?
Characterised by impaired insulin secretion and insulin resistance
94
TYPE 2 DIABETES what is the aetiology of T2DM?
- 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
95
TYPE 2 DIABETES Describe the pathophysiology of T2DM
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
96
TYPE 2 DIABETES Why is insulin secretion impaired in T2DM
Due to lipid deposition in the pancreatic islets
97
TYPE 2 DIABETES what are the risk factors for T2DM?
Increase w/ age M > F Ethnicity: African-Carribean, Black African and South Asian Obesity Hypertension
98
TYPE 2 DIABETES What happens to insulin resistance, insulin secretion and glucose levels in T2DM?
Insulin resistance increase Insulin secretion decreases Fasting and post-prandial glucose increase
99
TYPE 2 DIABETES Why do you rarely see diabetic ketoacidosis in T2DM?
Insulin secretion is impaired but there are still low levels of plasma insulin Low levels of insulin prevent muscle catabolism and ketogenesis
100
TYPE 2 DIABETES By how much has the beta cell mass reduced in T2DM when diagnosis usually occurs?
50% of normal beta cell mass
101
TYPE 2 DIABETES Describe the epidemiology of T2DM
Onset older (>30) Usually overweight More common in African/Asian populations Males > Females
102
TYPE 2 DIABETES Describe the treatment pathway for T2DM
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 5. Increase insulin dose as required
103
TYPE 2 DIABETES How does metformin work in treating T2DM?
Increase insulin sensitivity and inhibits glucose production
104
TYPE 2 DIABETES How does sulfonylurea work in treating T2DM?
Stimulates insulin release
105
TYPE 2 DIABETES Give a potential consequence of taking Sulfonylurea for the treatment of T2DM
Hypoglycaemia
106
REACTIVE ARTHRITIS What is reactive arthritis?
● A sterile synovitis which occurs following o A GI infection with Shigella, Salmonella, Yersinia or Campylobacter o Sexually acquired infection ● Typically affects lower limb
107
REACTIVE ARTHRITIS What GI infections are associated with causing reactive arthritis?
Salmonella Shigella Yersinia enterocolitica campylobacter
108
REACTIVE ARTHRITIS What GU infections are associated with causing reactive arthritis?
Chlamydia Ureaplasma urealyticum
109
REACTIVE ARTHRITIS What is the classic triad of symptoms for reactive arthritis?
1. Arthritis 2. Conjunctivitis 3. Urethritis (can't see, can't pee, can't climb a tree)
110
REACTIVE ARTHRITIS What investigations might you do in someone you suspect to have reactive arthritis?
ESR + CRP - raised ANA - negative RF - negative X-ray - sacroiliitis or enthesopathy Joint aspirate - negative (exclude septic arthritis + gout)
111
REACTIVE ARTHRITIS How is reactive arthritis treated?
NSAID Corticosteroids DMARD - chronic arthritis
112
FIBROMYALGIA What is the diagnostic criteria for fibromyalgia?
Chronic widespread pain lasting for > 3 months with other causes excluded Pain is at 11/18 tender point sites for 6 months
113
FIBROMYALGIA Name 4 diseases that fibromyalgia is commonly associated with
1. Depression 2. Choric fatigue 3. IBS 4. Chronic headache
114
FIBROMYALGIA Give 4 symptoms of fibromyalgia
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
115
FIBROMYALGIA Give 3 disease that might be included in the differential diagnosis for fibromyalgia
1. Hypothyroidism 2. SLE 3. Low vitamin D
116
FIBROMYALIGA How is fibromyalgia diagnosed?
Everything seems normal 11/18 trigger points Exclude other diagnoses
117
FIBROMYALGIA Describe the management of fibromyalgia
- Educate the patient and family - CBT and exercise programmes - reset pain thermostat - Acupuncture - Analgesics - tramadol, codeine - Low dose antidepressants (amitriptyline) and anticonvulsants (pregabalin)
118
FIBROMYALGIA what is the epidemiology of fibromyalgia?
women, poor socioeconomic status, 20-50 year old
119
FIBROMYALGIA what is the the pathophysiology of fibromyalgia?
Unknown, possibly pain perception/hyper excitability of pain fibres
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FIBROMYALGIA what are the complications of fibromyalgia?
- can really affect quality of life - anxiety, depression, insomnia - opiate addiction
121
FIBROMYALGIA what is fibromyalgia?
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
122
GOUT What is gout?
Crystal arthritis Inflammatory arthritis caused by hyperuricaemia and intra-articular sodium urate crystals
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GOUT Describe the epidemiology of gout?
● 5x more common in men ● Occurs rarely before young adulthood ● Rarely occurs in pre-menopausal females ● Often a family history
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GOUT What joint does gout most commonly affect?
Big toe metatarsophalangeal joint
125
GOUT Describe the pathophysiology of gout
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
126
GOUT Give 3 causes of gout
= 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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GOUT Name 3 common precipitants of a gout attack
1. Aggressive introduction of hypouricaemic therapy 2. Alcohol or shellfish binges 3. Sepsis, MI, acute severe illness 4. Trauma
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GOUT Name 4 diseases that someone with gout might have an increased risk of developing
1. Hypertension 2. CV disease - e.g. stroke 3. Renal disease 4. Type 2 diabetes
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GOUT what is the clinical presentation of gout?
SYMPTOMS inflamed joints - 1st metatarsal and distal interphalangeal often affected. SIGNS tophi- lumps of urate salts
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GOUT What are tophi?
Onion like aggregates of urate crystals with inflammatory cells. Proteolytic enzymes are released --> erosion
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GOUT What investigations might you do in a patient you think has gout?
Joint aspiration & polarised light microscopy (needle like negative birefringent crystals), Increased Urate on blood test X-ray = rat bite erosions
132
GOUT What is the aim of treatment for gout?
To get urate levels < 300 mol/L
133
GOUT How would you treat acute gout?
Ice packs and rest NSAIDS Colchicine = anti-gout medication Corticosteroids - IM or IA
134
GOUT Name 3 treatment options for gout
1. Lifestyle modifications - diet, weight loss, reduce alcohol 2. Allopurinol (xanthine oxidase inhibitor) 3. NSAIDs or colchicine IM prednisolone
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GOUT You see a patient with gout who is taking bendroflumethiazide. What drug might you replace this with to help treat their gout?
You would switch bendroflumethiazide to cosartan as bendroflumethiazide is a diuretic and so impairs urate excretion
136
GOUT Name 6 factors that can cause an acute attack of gout
1. Sudden overload 2. Cold 3. Trauma 4. Sepsis 5. Dehydration 6. Drugs
137
GOUT A patient presents with an acute mono-arthropathy of their big toe. What are the two main differential diagnoses?
1. Gout 2. Septic arthritis
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GOUT A patient presents with an acute mono-arthropathy of their big toe. What investigations might you do?
Joint aspirate If septic arthritis - high WCC and neutrophilia and bacteria on gram stain If gout - urate crystals
139
PSEUDOGOUT Describe the pathophysiology of pseudogout
Calcium pyrophosphate crystals are deposited on joint surfaces - produces the radiological appearance of chondrocalcinosis Crystals elicit an acute inflammatory response
140
PSEUDOGOUT What can cause pseudogout?
1. Hypo/hyperthyroidism 2. Haemochromatosis 3. Diabetes 4. Magnesium levels
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PSEUDOGOUT what is the clinical presentation of pseudogout?
SYMPTOMS hot, swollen, tender joint, usually knees SIGNS recent injury to the joint in the history Typically the wrists and knees
142
PSEUDOGOUT What investigations might you do in someone you suspect might have pseudogout?
Aspiration --> fluid for crystals and blood cultures = positive birefringent rhomboid crystals X-rays --> can show chondrocalcinosis
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PSEUDOGOUT What is the most likely differential diagnosis for pseudogout?
Infection
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PSEUDOGOUT Describe the treatment for pseudogout
- high dose NSAIDs - ibuprofen - Colchicine - anti-gout - IM prednisolone - Aspiration, intra-articular steroid injections
145
PSEUDOGOUT What kind of crystals do you see in pseudogout?
Positive birefringent calcium pyrophosphate rhomboid crystals
146
GOUT What kind of crystals do you see in gout?
Monosodium urate crystals = negatively birefringent
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PSEUDOGOUT What kind of crystals fo you see in pseudogout?
Calcium pyrophosphate crystals = positively birefringent
148
BPH What is benign prostatic hypertrophy (BPH)? Complications?
- Overgrowth of prostatic tissue in transitional (inner) zone which compresses prostatic urethra - Obstruction not relieved may get infection (stasis) or hydroureter/nephrosis
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BPH How does BPH present?
LUTS: - Storage Sx (FUN) = Frequency, Urgency, Nocturia - Voiding Sx (HIT) = Hesitancy, Intermittent flow, Terminal dribbling UTI secondary to stasis, acute or chronic retention
150
BPH What are some investigations for BPH?
- 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
BPH What is the conservative management of BPH?
- Avoid caffeine + alcohol - Relax when voiding + void twice in a row to aid emptying - Control urgency with distraction methods
152
BPH What 2 medications can be used in BPH and what is their mechanism of action?
- 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
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BPH What are the side effects of... i) alpha blockers? ii) 5-alpha reductase inhibitors?
i) Postural hypotension (vasodilation), dizziness, dry mouth ii) Erectile dysfunction, reduced libido, ejaculation issues
154
BPH What surgical options may be considered for BPH? Complications?
- Transurethral resection of prostate (TURP) - SEs = urethral stricture, retrograde ejaculation, prostate perforation - Retropubic prostatectomy if very large (open surgery)
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HAEMATURIA What can cause... i) transient or non-visible haematuria? ii) persistent non-visible haematuria? iii) other?
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
HAEMATURIA What investigations might you do for haematuria?
- Urine dipstick initially (persistent = present in 2/3 samples 2w apart) - Check renal function, ACR or PCR + BP
157
HAEMATURIA What would warrant an urgent referral regarding haematuria?
- ≥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
CKD Define chronic kidney disease
Long standing, usually progressive, impairment in renal function for more than 3 months
159
CKD How is CKD diagnosed?
- eGFR < 60mL/min/1.73m2, or: - eGFR < 90mL/min/1.73m2 + signs of renal damage, or: - Albuminuria > 30mg/24hrs (Albumin:Creatinine > 3mg/mmol)
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CKD Briefly describe the pathophysiology begins CKD
Hyper-filtration for nephrons that work --> glomerular hypertrophy and reduced arteriolar resistance --> raised intraglomerular capillary pressure and strain --> accelerates remnant nephron failure (progressive)
161
CKD Name 4 cause of CKD
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
CKD Give 3 signs of CKD
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
CKD What investigations might be done in someone who has CKD?
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
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CKD Describe the management of CKD
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
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PROSTATE CANCER Define prostate cancer
Adenocarcinoma in the peripheral zone of the prostate gland
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PROSTATE CANCER Where can prostate cancer metastasise to?
Lymph nodes and bone | Rarely = brain, liver, lung
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PROSTATE CANCER By what routes can prostate cancer spread?
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
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PROSTATE CANCER What can cause prostate cancer?
1. High testosterone levels | 2. Family history - 2/3x increased risk if 1st degree relative is affected
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PROSTATE CANCER what are the symptoms of prostate cancer?
1. LUTS 2. Bone pain, weight loss, night sweats anaemia = mets Most picked up in asymptomatic stage
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PROSTATE CANCER What investigations might you do in someone who you suspect has prostate cancer?
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
PROSTATE CANCER What grading system is used in prostate cancer?
Gleason grading = higher the score, the more aggressive the cancer
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PROSTATE CANCER What is the treatment for localised prostate cancer?
prostatectomy (<70), active surveillance (>70 and low risk), radiotherapy
173
PROSTATE CANCER What is the treatment for metastatic prostate cancer?
- chemotherapy, - radiotherapy, - bilateral orchidectomy (gold standard hormonal treatment), - Goserelin (LHRH receptor blocker), - palliative treatments focus on relieving symptoms e.g. TURP
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PROSTATE CANCER Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer
Advantages: 1. Curative 2. Reduced patient anxiety Disadvantages: 1. Can have adverse effects
175
PROSTATE CANCER How do LH antagonists work in treating prostate cancer?
First stimulate and then inhibit pituitary gonadotrophin E.g. Leuprolide
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PROSTATE CANCER Is a raised PSA confirmatory of prostate cancer?
NO Prostate cancer indication
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PROSTATE CANCER Other than prostate cancer, what can cause an elevated PSA?
1. Benign prostate enlargement 2. UTI 3. Prostatitis
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PROSTATE CANCER Give 2 advantages and 2 disadvantages of screening in prostate cancer
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
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PROSTSTE CANCER What is PSA?
A glycoprotein secreted by the prostate into the blood stream
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UTI Define urinary tract infection
Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria
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UTI What determines if a UTI is complicated or uncomplicated?
A UTI is deemed complicated if it affects: - Someone with an abnormal urinary tract - A man - Pregnant lady - Children - Immunocompromised - If it is recurrent
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UTI Describe the pathophysiology of UTI's
Organisms colonise the urethral meatus --> bacterial sent --> bacteriuria
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UTI Name 3 UTI causative organisms
1. Uropathogenic strains of E. coli (UPEC) - 82% 2. Coagulase negative staph (s. saprophyticus) 3. Proteus mirabilis 4. Enterococci 5. Klebsiella pneumonia
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UTI Describe the epidemiology of UTI's
More common in women due to short urethra and its proximity to the anus
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UTI Give 4 risk factors of UTI's
1. Catheter 2. Female 3. Prostatic hypertrophy (obstructs) 4. Low urine volume 5. Urinary tract stones 6. Pregnancy
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UTI Give 3 bacterial virulence factors that aid their ability to cause UTI's
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)
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UTI What type of pili would you associate with lower UTI?
Type 1 Bind to uroplakin
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UTI What type of pili would you associate with upper UTI?
Type P Bind to glycolipids on urothelium
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UTI The vagina is heavily colonised with lactobacilli, what is the function of this?
Helps maintain a low pH = host defence mechanism
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UTI Give 2 reasons why a post-menopausal women is more susceptible to a UTI
1. pH rises --> increased colonisation by colonic flora 2. Reduced mucus secretion
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UTI Give 3 host defence mechanisms against UTIs
1. Antegrade flushing of urine 2. Tamm-horsfall protein 3. GAG layer 4. Low urine pH 5. Commensal flora 6. Urinary IgA
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UTI Define pyuria
Presence of pus in urine
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UTI Name 4 lower urinary tract infections
1. Cystitis 2. Prostatitis 3. Epididymo-orchitis 4. Urethritis
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UTI Name a upper urinary tract infection
Pyelonephritis
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UTI Give 4 classic UTI symptoms
1. Urgency 2. Frequency 3. Dysuria 4. Haematuria 5. Abdominal pain 6. Malaise 7. Confusion (old patients)
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UTI What investigations might you do in someone who you suspect has a UTI?
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)
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UTI What is the first line treatment for an uncomplicated UTI?
Trimethoprim or nitrofurantoin for 3 days | Increase fluid intake and regular voiding
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UTI How does trimethoprim work?
It affects folic acid metabolism
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UTI Describe the management for a complicated UTI
Culture sample --> Abx for 7 days
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UTI Define recurrent UTI
>2 episodes in 6 months or >3 in 12 months
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UTI Describe the management for someone who is having recurrent UTIs
1. Increase fluid intake 2. Regular voiding 3. Void pre and post intercourse 4. Abx prophylaxis 5. Vaginal oestrogen replacement
202
ACNE VULGARIS what is it?
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.
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ACNE VULGARIS what is the pathophysiology?
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
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ACNE VULGARIS what is the clinical presentation of mild acne?
open and closed comedones with or without sparse inflammatory lesions
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ACNE VULGARIS what is the clinical presentation of moderate acne?
widespread non-inflammatory lesions and numerous papules and pustules
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ACNE VULGARIS what is the clinical presentation of severe acne?
extensive inflammatory lesions, which may include nodules, pitting, and scarring
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ACNE VULGARIS what is the management?
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
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ACNE VULGARIS what is a complication of long term antibiotics use and how can this be treated?
gram-negative folliculitis treated with high dose trimethoprim
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IMPETIGO what is impetigo and what is it caused by?
it is a superficial bacterial skin infection caused by staph. aureus or strep. pyogenes
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IMPETIGO where does it affect on the body?
anywhere but lesions tend to occur on face, flexures and limbs not covered by clothing
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IMPETIGO how is impetigo spread?
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.
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IMPETIGO what is the incubation time?
between 4 to 10 days.
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IMPETIGO what are the clinical features?
'golden', crusted skin lesions typically found around the mouth very contagious
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IMPETIGO what is the management?
- 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
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IMPETIGO hoe long should a child be excluded from school?
- until lesions are crusted and healed or 48 hours after commencing antibiotic treatment
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GLANDULAR FEVER what causes it?
EBV (also known as HHV-4) - most cases CMV HHV-6
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GLANDULAR FEVER what is the classic triad of symptoms?
- 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
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GLANDULAR FEVER what are the other symptoms?
malaise, anorexia, headache palatal petechiae splenomegaly hepatitis, transient rise in ALT lymphocytosis haemolytic anaemia secondary to cold agglutins (IgM) a maculopapular, pruritic rash
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GLANDULAR FEVER how long does it typically take for symptoms to resolve?
2-4 weeks
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GLANDULAR FEVER what are the investigations?
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.
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GLANDULAR FEVER what is the management?
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
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LYME DISEASE what is lyme disease caused by?
spirochaete Borrelia burgdorferi and is spread by tick
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LYME DISEASE what are the early features of lyme disease?
- erythema migrans - bulls eye rash, develops 1-4 weeks after bite, usually painless - headache - lethargy - fever - arthralgia
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LYME DISEASE what are the later features of lyme disease?
CVS - heart block - peri/myocarditis neurological - facial nerve palsy - radicular pain - meningitis
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LYME DISEASE what are the investigations?
- diagnosed clinically if erythema migrans is present - ELISA test - immunoblot for lyme disease
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LYME DISEASE what is the management of asymptomatic tick bites?
- if tick is still present, remove using fine tipped tweezers
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LYME DISEASE what is the management?
- doxycycline (amoxicillin if pregnant) - ceftriaxone in disseminated disease
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MEASLES what is it caused by?
RNA paramyxovirus
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MEASLES how is it spread and what is the incubation period?
- aerosol transmission - 10-14 days
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MEASLES when are you infectious with measles?
from prodrome to 4 days after the rash starts
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MEASLES what are the clinical features?
- 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
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MEASLES what are the investigations?
- IgM antibodies
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MEASLES what is the management?
mainly supportive admission may be considered in immunosuppressed or pregnant patients notifiable disease → inform public health
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MEASLES what are the complications?
- otitis media = most common - pneumonia = most common cause of death - encephalitis - subacute sclerosing panencephalitis - febrile convulsions - keratoconjunctivitis - diarrhoea
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MEASLES what is the management for contacts?
- if child is not immunised, MMR vaccine should be offered within 72 hours
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MUMPS what is mumps caused by?
RNA paramyxovirus
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MUMPS how is it spread and what is the incubation period?
- spread by droplets - incubation = 14-21 days
238
MUMPS when are you infectious?
7 days before and 9 days after parotid swelling starts
239
MUMPS what is the clinical presentation?
fever malaise, muscular pain parotitis ('earache', 'pain on eating'): unilateral initially then becomes bilateral in 70% parotid gland swelling
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MUMPS what is the management?
rest paracetamol for high fever/discomfort notifiable disease
241
MUMPS what are the complications?
- orchitis - hearing loss - usually unilateral and transient - meningoencephalitis - pancreatitis
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URTICARIA what is it?
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
URTICARIA what are the clinical features?
pale, pink raised skin. Variously described as 'hives', 'wheals', 'nettle rash' pruritic
244
URTICARIA what is the management?
non-sedating antihistamines are first-line prednisolone is used for severe or resistant episodes
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ANAPHYLAXIS what is it defined as?
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction.
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ANAPHYLAXIS what are the clinical features?
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
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ANAPHYLAXIS what are the most common causes?
food (e.g. nuts) - the most common cause in children drugs venom (e.g. wasp sting)
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ANAPHYLAXIS what is the emergency management?
500 micrograms IM adrenaline every 5 minutes IV fluid bolus
249
ANAPHYLAXIS what is refractory anaphylaxis?
defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline
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ANAPHYLAXIS what is the management of refractory anaphylaxis?
IV adrenaline infusion IV fluid boluses High flow oxygen If no response to adrenaline try noradrenaline, vasopressin
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ANAPHYLAXIS what is the management following initial stabilisation?
- non-sedating antihistamines - take serum tryptase levels - referral to allergy clinic - give 2x adrenaline injectors + training
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CONJUNCTIVITIS what are the different types?
It is commonly split into three categories: allergic viral bacterial
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CONJUNCTIVITIS what are the general clinical features?
- red, painful eye that may feel gritty/itchy - discharge - photophobia (suggests corneal involvement) - visual acuity should not be affected
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CONJUNCTIVITIS what are the clinical features of allergic conjunctivitis?
- serous discharge from eyes - conjunctival oedema in severe cases - symptoms are exacerbated at certain times of the year
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CONJUNCTIVITIS what is the cause of allergic conjunctivitis?
type 1 hypersensitivity reaction due to airborne allergens
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CONJUNCTIVITIS what is the management of allergic conjunctivitis?
conservative management avoid allergen artificial tears (dilutes allergen) antihistamines
257
CONJUNCTIVITIS what are the clinical features of viral conjunctivitis?
- serous discharge - more likely to be unilateral - more common than bacterial
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CONJUNCTIVITIS what is the management of viral conjunctivitis?
conservative prevent spread - hand hygiene and don't share towels artificial tears
259
CONJUNCTIVITIS what are the clinical features of bacterial conjunctivitis?
- purulent discharge - eyelids stuck together
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CONUNCTIVITIS what are the causes of bacterial conjunctivitis?
- staph. epidermis - staph. aureus - strep. pneumoniae - H. influenzae - chlamydia - gonorrhoea
261
CONJUNCTIVITIS what is the management of bacterial conjunctivitis?
- resolves within 7-14 days - topical chloramphenicol - lubricating eye drops
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INFLUENZA what are the different types of flu?
A, B and C different host organisms produce different strains
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INFLUENZA what type of virus is flu?
RNA single stranded virus
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INFLUENZA how is it transmitted?
via respiratory droplets
265
INFLUENZA what are the clinical features?
Fever ≥ 37.8°C Non-productive cough Myalgia Headache Malaise Sore throat Rhinitis
266
INFLUENZA what is the incubation period and infectious period for influenza?
incubation period = 1-4 days infectious period = 7-21 days
267
INFLUENZA what are the complications?
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
INFLUENZA how is it diagnosed?
PCR testing
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INFLUENZA what is the management?
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
INFLUENZA how can it be prevented?
vaccination - inactivated vaccine recommended for over 65, chronic condition, healthcare workers, nursing home residents
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BURSITIS what is it?
A painful condition where bursae of joints become inflamed
272
BURSITIS what are the most common locations?
shoulder elbow hip Often occurs near joints that experience repetitive movements
273
BURSITIS what are the symptoms?
Affected joint might: - feel achy or stiff - hurt more when moved or press on it - look swollen and red
274
BURSITIS what are the causes?
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
BURSITIS what are the risk factors?
- age - occupation - systemic conditions such as RA, gout and DM - obesity
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BURSITIS how can it be prevented?
- use kneeling pads - lift properly - take frequent breaks - weight loss - exercising
277
BURSITIS what are the investigations?
- clinical diagnosis - x-ray - USS or MRI - FBC with CRP, ESR
278
BURSITIS what is the management?
- anti-inflammatory - NSAIDs - antibiotics for infection - physiotherapy - corticosteroid injections - crutches to relieve pressure - surgical drainage
279
CONTACT DERMATITIS What is it?
type of eczema triggered by contact with a particular substance It usually improves/clears up if the substance causing the problem is avoided
280
CONTACT DERMATITIS what are the symptoms?
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
CONTACT DERMATITIS? what are the causes?
- 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
CONTACT DERMATITIS what are the investigations?
- clinical diagnosis - identification of irritants/allergens through history or patch testing
283
CONTACT DERMATITIS what is the management?
- avoid the cause - emollients - topical corticosteroids - steroid tablets if severe
284
CUTANEOUS WARTS what are the causes?
HPV infection This causes an excess amount of keratin to develop in the epidermis
285
CUTANEOUS WARTS are they contagious?
- 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
CUTANEOUS WARTS what are the symptoms?
- not usually painful - occasionally itch/bleed
287
CUTANEOUS WARTS? what are the different types?
- 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
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CUTANEOUS WARTS what is the management?
- will usually clear without treatment but can take up to 2 years to clear system - salicylic acid - cryotherapy - chemical treatment - formaldehyde, silver nitrate
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CUTANEOUS WARTS how can they be prevented?
- keep feet dry - change socks everyday - wear pool slippers/flip flops - cover wart to prevent spread to other people
290
FOLLICULITIS what is it?
common condition where hair follicles become inflamed
291
FOLLICULITIS what are the symptoms?
- 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
FOLLICULITIS what are the 2 main types?
- superficial - involves part of the follicle - deep - involves the entire follicle and is usually more severe
293
FOLLICULITIS what are the causes?
- staph aureus infection can also be caused by viruses, fungi, parasites medications or physical injury
294
FOLLICULITIS what are the risk factors?
- 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
FOLLICULITIS how can it be prevented?
- wash skin regularly - do laundry regularly - avoid friciton/pressure on skin - avoid shaving
296
FOLLICULITIS what is the management?
- antibiotic lotion - antifungal shampoos - creams to calm inflammation
297
BENIGN EYELID DISORDERS - BLEPHARITIS what is it?
- inflammation of the eyelid
298
BENIGN EYELID DISORDERS - BLEPHARITIS what are the symptoms?
- bilateral symptoms - ocular irritation - foreign body sensation - burning - redness - crusting
299
BENIGN EYELID DISORDERS - BLEPHARITIS what is the pathophysiology?
congestion and inflammation of eyelash follicles + meibomian glands
300
BENIGN EYELID DISORDERS - BLEPHARITIS what are the causes?
Atopic dermatitis (staphylococcal) Seborrheic dermatitis Acne rosacea Demodex infestation (mites)
301
BENIGN EYELID DISORDERS - BLEPHARITIS what is the management?
lid hygiene - warm compression, eyelid massage, cleaning eyelids topical antibiotic ointment low dose tetracyclines regular omega-3 supplements
302
BENIGN EYELID DISORDERS - STYE what is it?
infection of eyelash follicle also known as hordeolum
303
BENIGN EYELID DISORDERS - STYE what is the cause?
staph infection of eyelash follicle
304
BENIGN EYELID DISORDERS - STYE what are the symptoms?
tender red eyelash follicle swellings
305
BENIGN EYELID DISORDERS - STYE what is the management?
most self resolve - warm compression - removal of eyelash - incision with sterile needle - topical antibiotics (chloramphenicol) or co-amoxiclav PO if recurrent or severe
306
BENIGN EYELID DISORDERS - CHALAZION what is it?
granulomatous inflammation of an obstructed meibomian gland on internal eyelid
307
BENIGN EYELID DISORDERS - CHALAZION what are the causes?
- non-infectious - associated with blepharitis and acne rosacea
308
BENIGN EYELID DISORDERS - CHALAZION what are the symptoms?
painless red eyelid cysts in internal eyelid non-tender
309
BENIGN EYELID DISORDERS - CHALAZION what is the management?
often resolve spontaneously - warm compression + eyelid massage
310
BENIGN EYELID DISORDERS - ENTROPION what is it?
inward turning of eyelid
311
BENIGN EYELID DISORDERS - ENTROPION what are the causes?
- age-related degenerative changes - trachoma infection (chlamydia infection of eye)
312
BENIGN EYELID DISORDERS - ENTROPION what is the management?
- examination for corneal abrasions + ulcers - lubricants to reduce risk of abrasions/ulcers
313
BENIGN EYELID DISORDERS - ECTROPION what is it?
outward turning of the eyelid
314
BENIGN EYELID DISORDERS - ECTROPION what are the causes?
- age-related degenerative changes - facial nerve palsy (bell's palsy)
315
BENIGN EYELID DISORDERS - ECTROPION what is the clinical presentation?
sore red eye watery due to disrupted tear drainage
316
BENIGN EYELID DISORDERS - ECTROPION what is the management?
- eye lubrication drops - taping eyes shut at night - severe = surgery
317
BENIGN EYELID DISORDERS - ECTROPION what can this condition lead to?
exposure keratopathy - can cause sight loss
318
BENIGN EYELID DISORDERS - TRICHIASIS what is it?
when eyelashes grow inwards due to damaged eyelash follicles
319
BENIGN EYELID DISORDERS - TRICHIASIS what is the most common cause?
chronic blepharitis
320
BENIGN EYELID DISORDERS - TRICHIASIS whay is the management?
- epilating eyelashes (however they reoccur every few weeks) - electrolysis/laser ablation can destroy follicle

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