GP CONDITIONS Flashcards

1
Q

HTN
What is malignant HTN?

A

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

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2
Q

HTN
How might malignant HTN present?
Management?

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

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

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

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

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

A

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

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5
Q

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

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

A

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

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6
Q

HTN
In terms of HTN medication, what is…

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

A

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

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7
Q

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

A

Ramipril,

inhibit conversion of angiotensin I>II

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8
Q

HTN
What are the side effects of ACEi?

A

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

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9
Q

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

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

A

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

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10
Q

ANGINA
What is the secondary prevention of angina?

A

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

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11
Q

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

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

ACS
What are the complications following ACS?

A

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

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13
Q

ACS
What is the management of NSTEMI?

A

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

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14
Q

ACS
What is the secondary prevention of ACS?

A

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

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15
Q

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

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

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

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

CONSTIPATION
What is the management of constipation?

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

GALLSTONES
What causes gallstones?
Risk factors?

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

ACUTE CHOLECYSTITIS
What is the clinical presentation of acute cholecystitis?

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

ACUTE CHOLECYSTITIS
Investigations for acute cholecystitis?

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

ACUTE CHOLECYSTITIS
Management of acute cholecystitis?

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

PERIPHERAL VASCULAR DISEASE
what are the investigations for PVD?

A

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

<0.3 = critical ischaemia

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23
Q

ARRHYTHMIAS
Give 2 effects of hypokalaemia on an ECG

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

ARRHYTHMIAS
Give an effect of hypocalcaemia on an ECG

A
  1. QT prolongation
  2. T wave flattening
  3. Narrowed QRS
  4. Prominent U waves
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25
ARRHYTHMIAS Give an effect of hypercalcaemia on an ECG
1. QT shortening 2. Tall T wave 3. No P waves
26
ARRHYTHMIAS What ECG changes might you see with someone with ventricular tachycardia?
Crescendo-decrescendo amplitude = torsades de pointes
27
HEART BLOCK Describe a first degree heart block
Fixed prolongation of the PR interval due to delayed conduction to the ventricles - PR interval >0.22s - asymptomatic
28
HEART BLOCK Describe a second degree heart block
There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles
29
HEART BLOCK Describe a Mobitz type 1 second degree heart block
PR interval gradually increases until AV node fails and no QRS is seen PR interval returns to normal and the cycle repeats
30
HEART BLOCK Describe a Mobitz type 2 second degree heart block
Sudden unpredictable loss of AV conduction and so loss of QRS PR interval is constant but every nth QRS is missing wide QRS
31
HEART BLOCK Explain the pathophysiology of a BBB
Lack of simultaneous ventricular contractions LBBB = R before L RBBB = L before R
32
IBS Describe the pharmacological treatment of IBS
1. Antispasmoidics for bloating - mebeverine 2. Laxatives for constipation 3. Anti-motility agent for diarrhoea - loperamide 4. Tricyclic antidepressants
33
HTN What is an example and mechanism of action of CCB?
Amlodipine, act on L-type Ca2+ channels
34
HTN What is an example and mechanism of action of thiazide-like diuretic?
Indapamide, locks Na+ reabsorption at DCT by blocking Na+/Cl- symporter
35
HTN What is an example and mechanism of action of ARB?
Candesartan, blocks effects of angiotensin II at the AT1 receptor
36
HTN What are the side effects of CCB?
Oedema, headache, flushing palpitations
37
HTN Name 4 classes of diuretics
1. Thiazides 2. Loop 3. Potassium sparing 4. Aldosterone antagonists
38
HTN What are the side effects of beta-blocker?
Headache, hypotension, erectile dysfunction
39
HTN What are the risk factors for HTN?
Modifiable: - alcohol intake - sedentary lifestyle - diabetes mellitus - sleep apnoea - smoking Non-modifiable: - Increasing age - family history - ethnicity - afro-Caribbean
40
HTN Where in the kidney do thiazide diuretics work?
The distal tubule
41
ACS Give 3 signs of MI
1. Hypo/hypertension 2. 3rd/4th heart sound 3. Signs of congestive heart failure 4. Ejection systolic murmur
42
ACS How does aspirin work?
Antiplatelet Irreversibly inhibits COX --> reduced thromboxane 2 synthesis --> platelet aggregation reduced
43
ACS How does clopidogrel work?
Antiplatelet P2Y12 inhibitor --> prevents platelet activation
44
OTITIS EXTERNA What is malignant otitis externa?
- Immunocompromised, DM or elderly where it can spread to the surrounding bones (mastoid + temporal)
45
OTITIS EXTERNA What are some causes of otitis externa?
- Infection (staph. aureus, pseudomonas aeruginosa or fungal) - Seborrhoeic dermatitis - Contact dermatitis (allergic + irritant)
46
OTITIS EXTERNA What is the management of otitis externa?
- 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
47
T2DM What is the pathophysiology of T2DM?
- 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
48
T2DM What values are diagnostic for T2DM?
- 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
49
T2DM What is a main complication of uncontrolled T2DM?
- Hyperglycaemic hyperosmolar state - Decrease insulin = increase serum glucose + serum osmolality + urination but no ketosis as still some endogenous insulin
50
T2DM How does HHS present? How is it diagnosed? Management?
- Marked dehydration (polydipsia, polyuria, hypovolaemia) + impaired consciousness - Plasma glucose >30mmol/L, plasma osmolality >320mOsm - IV fluid replacement, infuse insulin, LMWH prophylaxis as hyperviscous blood
51
T2DM List 6 medications that can be used in T2DM
- Metformin (biguanide, first line) - Gliclazide (sulfonylurea) - Sitagliptin (DPP4 inhibitor) - Empagliflozin (SGLT) - Glitazone (pioglitazone) - GLP-1 mimetics
52
T2DM What is the mechanism of action of... i) metformin? ii) gliclazide? iii) sitagliptin?
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
53
T2DM What is the mechanism of action of... i) empagliflozin? ii) glitazone? iii) GLP-1 mimetics?
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)
54
T2DM What are some side effects of... i) metformin? ii) gliclazide? iii) sitagliptin? iv) empagliflozin? v) glitazone? vi) GLP-1 mimetics?
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
55
HYPERTHYROIDISM What are the 3 mechanisms explaining the causes of hyperthyroidism?
- Overproduction of thyroid hormone - Leakage of pre-formed hormone from thyroid - Ingestion of excess thyroid hormone
56
HYPERTHYROIDISM What are some other causes of hyperthyroidism?
- Toxic multinodular goitre = nodules secrete excess thyroid hormones (elderly women) - Toxic adenoma = solitary nodule producing T3/4 - DeQuervain's thyroiditis = acute inflammation - Exogenous iodine (food, amiodarone)
57
HYPERTHYROIDISM What are the Graves' disease specific features?
- Diplopia, ophthalmoplegia, increased tears - Exophthalmos, lid lag + retraction - Thyroid acropachy (clubbing, painful digits) - Pretibial myxoedema
58
HYPERTHYROIDISM What are some investigations for hyperthyroidism?
- TFTs (primary = low TSH, high T3/4, secondary = high TSH, high T3/4 hypothalamus or pituitary pathology) - Thyroid autoantibodies - Isotope scan
59
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
60
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
61
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)
62
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)
63
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
64
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
65
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
66
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)
67
PSEUDOGOUT What is the management of pseudogout?
- NSAIDs, colchicine - Intra-articular steroids or PO - Joint aspiration of arthrocentesis if severe
68
PMR What is the management of PMR?
- ESR/CRP raised, CK normal - PO prednisolone shows dramatic response (diagnostic)
69
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
70
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
71
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
72
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
73
TYPE 2 DIABETES Why is insulin secretion impaired in T2DM
Due to lipid deposition in the pancreatic islets
74
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
75
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
76
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
77
TYPE 2 DIABETES How does metformin work in treating T2DM?
Increase insulin sensitivity and inhibits glucose production
78
TYPE 2 DIABETES How does sulfonylurea work in treating T2DM?
Stimulates insulin release
79
TYPE 2 DIABETES Give a potential consequence of taking Sulfonylurea for the treatment of T2DM
Hypoglycaemia
80
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)
81
REACTIVE ARTHRITIS How is reactive arthritis treated?
NSAID Corticosteroids DMARD - chronic arthritis
82
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
83
FIBROMYALGIA Name 4 diseases that fibromyalgia is commonly associated with
1. Depression 2. Choric fatigue 3. IBS 4. Chronic headache
84
FIBROMYALGIA Give 3 disease that might be included in the differential diagnosis for fibromyalgia
1. Hypothyroidism 2. SLE 3. Low vitamin D
85
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)
86
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
87
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
88
PSEUDOGOUT What can cause pseudogout?
1. Hypo/hyperthyroidism 2. Haemochromatosis 3. Diabetes 4. Magnesium levels
89
PSEUDOGOUT What kind of crystals do you see in pseudogout?
Positive birefringent calcium pyrophosphate rhomboid crystals
90
GOUT What kind of crystals do you see in gout?
Monosodium urate crystals = negatively birefringent
91
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
92
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
93
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
94
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
95
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)
96
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)
97
CKD What are the different stages of CKD?
Stage 1 = <90 Stage 2 = 60-89 Stage 3a = 45-59 Stage 3b = 30-44 Stage 4 = 15-29 Stage 5 = <15
98
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)
99
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
100
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)
101
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
102
PROSTATE CANCER Define prostate cancer
Adenocarcinoma in the peripheral zone of the prostate gland
103
PROSTATE CANCER Where can prostate cancer metastasise to?
Lymph nodes and bone | Rarely = brain, liver, lung
104
PROSTATE CANCER What can cause prostate cancer?
1. High testosterone levels | 2. Family history - 2/3x increased risk if 1st degree relative is affected
105
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
106
PROSTATE CANCER What grading system is used in prostate cancer?
Gleason grading = higher the score, the more aggressive the cancer
107
PROSTATE CANCER Other than prostate cancer, what can cause an elevated PSA?
1. Benign prostate enlargement 2. UTI 3. Prostatitis
108
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
109
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
110
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
111
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
112
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
113
LYME DISEASE what is lyme disease caused by?
spirochaete Borrelia burgdorferi and is spread by tick
114
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
115
LYME DISEASE what are the later features of lyme disease?
CVS - heart block - peri/myocarditis neurological - facial nerve palsy - radicular pain - meningitis
116
LYME DISEASE what are the investigations?
- diagnosed clinically if erythema migrans is present - ELISA test - immunoblot for lyme disease
117
LYME DISEASE what is the management?
- doxycycline (amoxicillin if pregnant) - ceftriaxone in disseminated disease
118
ANAPHYLAXIS what is the emergency management?
500 micrograms IM adrenaline every 5 minutes IV fluid bolus
119
ANAPHYLAXIS what is refractory anaphylaxis?
defined as respiratory and/or cardiovascular problems persist despite 2 doses of IM adrenaline
120
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
121
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
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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
125
CONJUNCTIVITIS what is the management of bacterial conjunctivitis?
- resolves within 7-14 days - topical chloramphenicol - lubricating eye drops
126
BURSITIS what are the symptoms?
Affected joint might: - feel achy or stiff - hurt more when moved or press on it - look swollen and red
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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
128
BURSITIS what are the risk factors?
- age - occupation - systemic conditions such as RA, gout and DM - obesity
129
BURSITIS how can it be prevented?
- use kneeling pads - lift properly - take frequent breaks - weight loss - exercising
130
BURSITIS what are the investigations?
- clinical diagnosis - x-ray - USS or MRI - FBC with CRP, ESR
131
BURSITIS what is the management?
- anti-inflammatory - NSAIDs - antibiotics for infection - physiotherapy - corticosteroid injections - crutches to relieve pressure - surgical drainage
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FOLLICULITIS what are the causes?
- staph aureus infection can also be caused by viruses, fungi, parasites medications or physical injury
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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
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FOLLICULITIS what is the management?
- antibiotic lotion - antifungal shampoos - creams to calm inflammation
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BENIGN EYELID DISORDERS - BLEPHARITIS what are the causes?
Atopic dermatitis (staphylococcal) Seborrheic dermatitis Acne rosacea Demodex infestation (mites)
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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