Phase 2a things Flashcards

(129 cards)

1
Q

End Stage Renal Failure Levels:

A

Stage 1: > 90 mL/min/ 1.73m2
Stage 2: 60-89
Stage 3A: 45-59
Stage 3B: 30-44
Stage 4: 15-29
Stage 5/ESRF: <15

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2
Q

Gastric Ulcer vs Duodenal Ulcer

A

Gastric: pain immediately after eating
Duodenal: relived by eating, pain comes a while after eating

H. Pylori: 1 PPI + 2 antibiotics

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3
Q

AKI stages and causes

A

Stages of AKI:
1:
Creatinine is 1.5-1.9 times higher than baseline
urine output < 0.5ml/kg for > 6 consecutive hours

2:
Creatinine is 2-2.9 times higher than baseline
urine output < 0.5ml/kg for > 12 consecutive hours

3:
Creatinine is >3 times higher than baseline
Urine output < 0.5ml/kg for > 24 consecutive hours
Anuria for > 12 hours

NSAIDS, ACEi, ARBs, CCBs, a-blockers, b-blockers, opioids, diuretics, acyclovir, trimethoprim, lithium and more can cause AKIs

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4
Q

Renal Colic investigations

A

1st: USS
Diagnostic: CTKUB (CT scan of Kidneys, Ureter, Bladder)

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5
Q

Conns Syndrome

A

Causing primary hyperaldosteronism

Aldosterone acts on the kidneys to increase sodium absorption and as a result causes potassium excretion leading to Hypernatremia and hypokalaemia

The management is a potassium-sparing diuretic like spironolactone.

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6
Q

Varicose Veins: RF

A
  • old
  • female
  • pregnancy: the uterus causes compression of the pelvic veins
  • obesity
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7
Q

Varicose Veins: Pathophysiology

A
  • dilated, tortuous, superficial veins that occur secondary to incompetent venous valves, allowing blood to flow back, away from the heart
  • most commonly occur in the legs due to reflux in the great saphenous vein and small saphenous vein
  • extremely common, but most patients do not require intervention
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8
Q

Varicose Veins: S+S

A
  • aching, throbbing
  • itching
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9
Q

Varicose Veins: Complications

A
  • varicose eczema (aka venous stasis)
  • haemosiderin deposition → hyperpigmentation
  • lipodermatosclerosis → hard/tight skin
  • atrophie blanche → hypopigmentation
  • bleeding
  • superficial thrombophlebitis
  • venous ulceration
  • DVT
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10
Q

Varicose Veins: Investigations

A
  • venous duplex ultrasound: shows retrograde venous flow
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11
Q

Varicose Veins: Management

A

Conservative:
- leg elevation
- weight loss
- regular exercise
- graduated compression stockings

Referral to secondary care:
- pain, discomfort, swelling
- previous bleeding from varicose veins
- skin changes secondary to chronic venous insufficiency (e.g. pigmentation and eczema)
- superficial thrombophlebitis
- venous leg ulcer

Treatments:
- endothermal ablation: using either radiofrequency ablation or endovenous laser treatment
- foam sclerotherapy: irritant foam → inflammatory response → closure of the vein
- surgery: either ligation or stripping

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12
Q

Venous Ulceration

A
  • typically above medial malleolus

Investigations:
- ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing
- ‘normal’ ABPI: 0.9 - 1.2
- < 0.9 indicate arterial disease (or >1.3 as could be false-negative results from arterial calcification in diabetics)

Management
- compression bandaging, four layer [best]
- oral pentoxifylline: peripheral vasodilator
- little evidence for: flavinoids, hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression

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13
Q

Peripheral Arterial Disease: 3 main patterns of presentation

A

intermittent claudication
critical limb ischaemia
acute limb-threatening ischaemia

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14
Q

Peripheral Arterial Disease: Intermittent Claudication

A

S+S:
- intermittent claudication: aching or burning in the leg muscles following walking
- can walk a predictable distance before symptoms start
- relieved within minutes of stopping, not present at rest

Investigations:
- 1st: duplex ultrasound
- femoral, popliteal, posterior tibialis and dorsalis pedis pulses
- ankle brachial pressure index (ABPI): 1 = normal, <0.6= claudication
- magnetic resonance angiography (MRA) should be performed prior to any intervention

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15
Q

Peripheral Arterial Disease: Critical Limb Ischaemia

A

Features should include 1 or more of:
- rest pain in foot for more than 2 weeks
- ulceration
- gangrene
- hanging legs out of bed can ease pain

ABPI < 0.5 = critical limb ischaemia

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16
Q

Peripheral Arterial Disease: Acute Limb-threatening Ischaemia

A

Features - 1 or more of the 6 P’s
- pale
- pulseless
- painful
- paralysed
- paraesthetic
- ‘perishing with cold’

Investigations
- Doppler arterial
- ABPI
- Determine whether ischaemia is due to thrombus (rupture of atherosclerotic plaque) or embolus (e.g. secondary to atrial fibrillation)

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17
Q

Peripheral Artery Disease: Management

A

Lifestyle
- quit smoking
- comorbidities: HTN, DM, obesity
- exercise training
- clopidogrel + atorvastatin

Medical
- naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life

Surgical
- endovascular revascularization/angioplasty with stent (<10cm stenosis)
- surgical revascularization/bypass/endarterectomy (>10cm stenosis)
- amputation

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18
Q

Polymyalgia Rheumatica

A
  • Relatively common condition seen in older people
  • Characterised by muscle stiffness and raised inflammatory markers
  • Related to temporal arteritis + vasculitis

S+S:
- typically > 60 years old
- rapid onset (e.g. < 1 month)
- aching, morning stiffness in proximal limb muscles
- weakness is not considered a symptom of PMR
- mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats

Investigations
- ESR > 40 mm/hr
- Creatine kinase and EMG normal

Treatment
- prednisolone (should be very effective, if not consider DD)

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19
Q

Osteoarthritis: RF

A

F>M 3:1
Rare before 55yrs
Previous trauma
Obesity
Hypermobility
Occupation
Osteoporosis reduces the risk of OA

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20
Q

Osteoarthritis: Pathophysiology

A

“Wear and Tear”
- localised loss of cartilage
- remodelling of adjacent bone
- associated inflammation

Affects:
Large weight-bearing joints (hip, knee)
Carpometacarpal joint
DIP, PIP joints

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21
Q

Osteoarthritis: S+S

A
  • Asymmetric/Unilateral
  • Episodic joint pain: intermittent ache provoked by movement and relieved by resting
  • Transient morning stiffness <30 min (vs in RA)
  • Painless bony swellings: (osteophyte formation)
    • Heberden’s nodes at DIPD
    • Bouchard’s nodes at PIPD
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22
Q

Osteoarthritis: Investigations

A

X-Ray: (LOSS)
- Loss of joint space
- Osteophytes
- Subarticular sclerosis
- Subchondral cysts

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23
Q

Osteoarthritis: Management

A
  • Lifestyle: weight loss, exercise, walking aids
  • 1st: topical NSAIDs
  • 2nd: oral NDAIDs +ppi
  • intra-articular steroid injections
  • arthroplasty (joint replacement)
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24
Q

Rheumatoid Arthritis: RF

A
  • HLA DR4 and HLA DR1
  • can present anytime: any age (OA=old)
  • smoking
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25
Rheumatoid Arthritis: Pathophysiology
- chronic systemic autoimmune disorder causing symmetrical deforming autoimmune polyarthritis - primarily synovial disease Affects: - MCP, PIP joints
26
Rheumatoid Arthritis: S+S
- Symmetrical, bilateral - Swollen, painful joints in hands and feet, improves on movement - Morning Stiffness - Develops over months - Positive 'squeeze test' - discomfort on squeezing across the metacarpal or metatarsal joints - Hand deformities - Ulnar deviation - Swan neck/z thumb (P extension, D flexion) - Boutonnier deformity (P flexion, D extension Ocular manifestations - keratoconjunctivitis sicca (most common)
27
Rheumatoid Arthritis: Investigations
Bloods - Rheumatoid factor (also +ve in Felty, Sjogrens, IE, SLE) - Anti-cyclic citrullinated peptide antibody (higher specificity) - DAS28 monitor RA X ray - loss of joint space - juxta-articular osteoporosis - soft-tissue swelling - periarticular erosions - subluxation
28
Rheumatoid Arthritis: Management
DMARD monotherapy +/- a short-course of bridging prednisolone - Methotrexate: monitor FBC & LFT: risk of myelosuppression, liver cirrhosis, pneumonitis - Sulfasalazine - Leflunomide - Hydroxychloroquine TNF inhibitors: if 2 DMARDs fail - etanercept - infliximab - adalimumab - rituximab
29
Rheumatoid Arthritis: Complications
Extra-articular complications: - respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy - ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy - osteoporosis - ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus - increased risk of infections - depression Less common - Felty's syndrome (RA + splenomegaly + low white cell count) - amyloidosis
30
Rheumatoid Arthritis: pregnancy
- patients with early or poorly controlled RA should be advised to defer conception until disease is more stable - RA symptoms tend to improve in pregnancy but only resolve in a small minority. Patients tend to have a flare following delivery - methotrexate is not safe in pregnancy and needs to be stopped at least 6 months before conception - leflunomide is not safe in pregnancy - sulfasalazine and hydroxychloroquine are considered safe in pregnancy - low-dose corticosteroids may be used in pregnancy to control symptoms - NSAIDs may be used until 32 weeks but after this time should be withdrawn due to the risk of early close of the ductus arteriosus - patients should be referred to an obstetric anaesthetist due to the risk of atlanto-axial subluxation
31
Gout: RF
- males - purine-rich food: alcohol, red meat, liver, seafood, high fructose (sweets, fruit), saturated fats - drugs (aspirin, thiazide, loop diuretics) - FH - renal CKD (reduce uric acid excretion) - increased production from lymphoma, leukaemia, haemolysis, rhabdomyolysis
32
Gout: Pathophysiology
- inflammatory arthritis associated with hyperuricaemia and intra-articular monosodium urate crystals - purines need to be excreted as uric acid (hypoxanthine → xanthine → uric acid with enzyme xanthine oxidase) Lesch-Nyhan syndrome - hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency - x-linked recessive therefore only seen in boys - features: gout, renal failure, neurological deficits, learning difficulties, self-mutilation
33
Gout: S+S
Episodes lasting several days when their gout flares and are often symptom-free between episodes - pain: significant - swelling - erythema - tophaceous gout: persistently high uric acid can become chronic if monosodium urate form tophi on skin or joints, also release proteolytic enzymes leading to bone erosion
34
Gout: Investigations
Joint fluid aspiration + Microscopy: (diagnostic) - needle shaped negatively birefringent monosodium urate crystals under polarised light - increased leucocytes - >360 serum uric acid in acute settings X ray - joint effusion is an early sign - well-defined 'punched-out' erosions with sclerotic margins in a juxta-articular distribution, often with overhanging edges - relative preservation of joint space until late disease - eccentric erosions - no periarticular osteopenia (in contrast to rheumatoid arthritis) - soft tissue tophi may be seen
35
Gout: Management
1st: weight loss + lifestyle + vit Cm avoid some foods Acute Gout: - NSAIDs + ppi + Colchicine - Colchicine: inhibits microtubule polymerization by binding to tubulin, interfering with mitosis + inhibits neutrophil motility and activity, avoid if eGFR < 10 ml/min BNF - Intra-articular steroid injection Chronic Gout: - allopurinol: inhibits xanthine oxidase - febuxostat as alternative
36
Pseudogout "acute calcium pyrophosphate crystal deposition disease"
microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium Mostly >60, if <60, mostly likely has: - haemochromatosis - hyperparathyroidism - low magnesium, low phosphate - acromegaly, Wilson's disease Investigations: - knee, wrist and shoulders most commonly affected - joint aspiration: weakly-positively birefringent rhomboid-shaped crystals, radio-opaque (gout= radiolucent) - x-ray: chondrocalcinosis (in the knee this can be seen as linear calcifications of the meniscus and articular cartilage) Management - aspiration of joint fluid, to exclude septic arthritis - NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
37
Trochanteric Bursitis
Greater trochanteric pain syndrome is also referred to as trochanteric bursitis. It is due to repeated movement of the fibroelastic iliotibial band and is most common in women aged 50-70 years. Features pain over the lateral side of hip/thigh tenderness on palpation of the greater trochanter
38
Fibromyalgia
Syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites. Unknown cause RF: women 5x, 30-50yrs S+S: - chronic pain: at multiple site, sometimes 'pain all over' - lethargy - cognitive impairment: 'fibro fog' - sleep disturbance, headaches, dizziness are common Investigations: - tender in at least 11 of these 18 points stated Management: - explanation - aerobic exercise: has the strongest evidence base - cognitive behavioural therapy - medication: pregabalin, duloxetine, amitriptyline
39
Muscular Dystrophy
1. Duchenne MD – one of the most common and severe forms, it usually affects boys in early childhood; people with the condition will usually only live into their 20s or 30s 2. Becker MD – closely related to Duchenne MD, but it develops later in childhood and is less severe; life expectancy isn't usually affected as much 3. myotonic dystrophy – a type of MD that can develop at any age; life expectancy isn't always affected, but people with a severe form of myotonic dystrophy may have shortened lives 4. facioscapulohumeral MD – a type of MD that can develop in childhood or adulthood; it progresses slowly and isn't usually life-threatening 5. limb-girdle MD – a group of conditions that usually develop in late childhood or early adulthood; some variants can progress quickly and be life-threatening, whereas others develop slowly 6. oculopharyngeal MD – a type of MD that doesn't usually develop until a person is between 50 and 60 years old, and doesn't tend to affect life expectancy 7. Emery-Dreifuss MD – a type of MD that develops in childhood or early adulthood; most people with this condition will live until at least middle age
40
Reactive Arthritis/Reiter's syndrome
Reiter's Triad: urethritis, conjunctivitis and arthritis (can't pee, see, climb trees) Caused by distant infection, usually STI/GI - Shigella - Salmonella - Yersinia enterocolitica - Campylobacter - Chlamydia trochomatis Management - symptomatic: analgesia, NSAIDS, intra-articular steroids - sulfasalazine and methotrexate are sometimes used for persistent disease - symptoms rarely last more than 12 months
41
Discoid Meniscus: Pathophysiology, S+S
- A congenital anomaly of the knee in which the meniscus, instead of having the usual crescent (C-shape), is abnormally thickened and disc-shaped - More common in children and adolescents and typically affects the lateral meniscus of the knee. Anatomical Variation: - A discoid meniscus covers a larger portion of the tibial plateau compared to the normal meniscus - It is less flexible and more prone to injury S+S: Clicking or snapping sensation in the knee. Pain: Especially after activity. Swelling or stiffness of the knee. Mechanical symptoms: Locking or giving way of the knee
42
Discoid Meniscus: Investigations + Management
Types (Watanabe Classification): Type I (Complete): Fully disc-shaped and more prone to tearing. Type II (Incomplete): Partially disc-shaped. Type III (Wrisberg): Normal-shaped meniscus but lacks posterior attachments, leading to hypermobility. Investigations: - MRI: Preferred method to visualize the discoid shape and identify any associated tears. - X-ray: May show widened joint space if the discoid meniscus is thickened Management: - Conservative for asymptomatic or mildly symptomatic cases - Physical therapy to improve knee strength and stability. - Surgical Treatment if symptomatic + tear present: Meniscectomy or Meniscoplasty
43
Infectious mononucleosis (glandular fever)
Causes: - Epstein-Barr virus (EBV, aka human herpesvirus 4, HHV-4): 90% causes - Others: cytomegalovirus and HHV-6 - most common in adolescents and young adults S+S: resolves 2-4 weeks Triad: 1. sore throat, 2. pyrexia, 3. lymphadenopathy (posterior triangles of the neck, vs tonsillitis only in upper anterior cervical chain) - malaise, anorexia, headache - palatal petechiae - splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture - hepatitis, transient rise in ALT - lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes - haemolytic anaemia secondary to cold agglutins (IgM) - a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis Diagnosis - heterophil antibody test (Monospot test) - FBC - do both in 2nd week of the illness to confirm a diagnosis Management Supportive treatment: rest during the early stages, drink plenty of fluid, avoid alcohol, simple analgesia for any aches or pains - Avoid contact sports for 4 weeks to reduce risk of splenic rupture Complications - Splenic rupture - Hepatitis/pericarditis/myocarditis - HUS
44
Lyme Disease: S+S, Investigations
Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks. Early features (within 30 days) - erythema migrans: - 'bulls-eye' rash at the site of the tick bite - 1-4 weeks after the initial bite - painless, > 5 cm diameter, slowly increases size - systemic features: headache, lethargy, fever, arthralgia Later features (after 30 days) - cardiovascular - heart block - peri/myocarditis - neurological - facial nerve palsy - radicular pain Investigations - Can be diagnosed clinically if erythema migrans - 1st: ELISA antibodies to Borrelia burgdorferi, repeat after 4-6 weeks if negative but still suspected - if positive/12 weeks of sx, do immunoblot test
45
Lyme Disease: Management
Management of asymptomatic tick bites - if the tick is still present, remove with fine-tipped tweezers + wash - NICE guidance does not recommend routine antibiotic treatment to patients who've suffered a tick bite Management of suspected/confirmed Lyme disease - doxycycline (amoxicillin if CI) - Erythema migrans → commenced on antibiotic asap ceftriaxone if disseminated disease - Jarisch-Herxheimer reaction (fever, rash, tachycardia after first dose of antibiotic) can be seen
46
Contact dermatitis
There are two main types of contact dermatitis 1. irritant contact dermatitis: common - non-allergic reaction due to weak acids or alkalis (e.g. detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare 2. allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid is indicated Cement is a frequent cause of contact dermatitis. The alkaline nature of cement may cause an irritant contact dermatitis whilst the dichromates in cement also can cause an allergic contact dermatitis
47
Squamous Cell Carcinoma
Squamous cell carcinoma is a common variant of skin cancer. Metastases are rare but may occur in 2-5% of patients. RF: - sunlight / psoralen UVA exposure - actinic keratoses and Bowen's disease - immunosuppression e.g. renal transplant, HIV - smoking - long-standing leg ulcers (Marjolin's ulcer) - genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism S+S - sun-exposed sites such as head, neck, dorsum hands and arms - rapidly expanding painless, ulcerate nodules - possible cauliflower-like appearance - possible bleeding Invsetigations: - Surgical excision (4mm or 6mm margins if >20mm diameter) - Mohs micrographic surgery: high-risk patients/cosmetic Poor prognosis: - poorly differentiated, >20mm diameter, >4mm deep, immunosupression
48
Ulcerative Colitis
Peak incidence: 15-25 yrs, 55-65 yrs RF: stress, NSAIDs, antibiotics, NOT smoking S+S bloody diarrhoea urgency tenesmus abdominal pain, particularly in the left lower quadrant extra-intestinal features: APIESAC (Ankylosing spondolitis, Pyoderma gangrenosum, Iritis, Erythema nodosum, Sclerosing cholangitis, Aphthous ulcers/Amyloidosis, Clubbing)
49
Ulcerative Colitis: Investigations
Colonoscopy + biopsy: - red, raw mucosa, bleeds easily - no inflammation beyond submucosa (only colonic mucosa + submucosa affected) - widespread ulceration with pseudopolyps - inflammatory infiltrate - crypt abscesses (neutrophils) - goblet cell depletion - avoided in severe colitis colonoscopy: risk of perforation - a flexible sigmoidoscopy preferred Barium enema: - loss of haustrations - superficial ulceration, 'pseudopolyps' - long-standing disease: colon is narrow and short -'drainpipe colon' Bloods - pANCA (anti-neutrophilic cytoplasmic antibody) +ve (-ve in Crohn's) - high ESR, CRP, WCC, platelets - low albumin - fecal calprotectin increased (normal in IBS)
50
Ulcerative Colitis: Management
mild: < 4 stools/day, only a small amount of blood moderate: 4-6 stools/day, varying amounts of blood, no systemic upset severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers) Inducing remission: mild + moderate - topical aminosalicylate: rectal mesalazine - + oral aminosalicylate - + topical or oral corticosteroid - if severe: hospital tx, IV steroids/IV ciclosporin, surgery (proctocolectomy with ileostomy) Maintaining remission - aminosalicylate - oral azathioprine/mercaptopurine (immunosupressant)
51
Crohn's Disease: RF, Pathophysiology
RF: Genetic (NOD2, CARD15, HLA-B27), smoking, NSAIDs, stress, late adolescence/early adulthood - Commonly terminal ileum and colon but can be anywhere from mouth to anus - inflammation occurs in all layers, down to the serosa: prone to strictures, fistulas, adhesions Distribution: 80%: small bowel, usually ileum 50%: ileocolitis 20%: colitis exclusively 30%: perianal
52
Crohn's Disease: S+S
- Weight loss, lethargy - Diarrhoea (less bloody than UC), but colitis may cause bloody, stetorrhoea - Abdominal pain: the most prominent symptom in children - Extra-intestinal features more common in colitis or perianal disease (arthritis, pyoderma gangrenosum, erythema nodosum)
53
Crohn's Disease: Investigations
Bloods - ESR, CRP, WCC, platelets - pANCA -ve (positive in UC) Endoscopy - colonoscopy + biopsy: deep ulcers, skip lesions, cobblestone appearance - inflammation in all layers from mucosa to serosa - goblet cells - granulomas Small bowel enema - high sensitivity and specificity for examination of the terminal ileum - strictures: 'Kantor's string sign' - proximal bowel dilation - 'rose thorn' ulcers - fistulae
54
Crohn's Disease: Management
Lifestyle: stop smoking Inducing remission - Glucocorticoids (oral/topical/IV): prednisolone - Enteral feeding with elemental diet if steroid intolerance (eg. children) - 2nd: 5-ASA drugs: mesalazine (not as effective) - + azathioprine/mercaptopurine - + infliximab - + metronidazole Maintaining remission - 1st: azathioprine/mercaptopurine: check +TPMT (thiopurine methyltransferase) activity before starting - 2nd: methotrexate (not used in UC) Surgery (in 80%) - stricturing terminal ileal disease → ileocaecal resection - segmental small bowel resections - stricturoplasty
55
Crohn's Disease: Complications
Perianal fistulae - an inflammatory tract or connection between the anal canal and the perianal skin - MRI to confirm - oral metronidazole/infliximab - draining seton (surgical thread) Perianal abscess - requires incision and drainage + antibiotics Risk of - small bowel cancer - colorectal cancer - osteoporosis
56
Coeliac Disease: RF
RF: associations with dermatitis herpetiformis, autoimmune disorders (T1DM, autoimmune hepatitis), HLA-DQ2/DQ8, if children then <3 after cereals Autoimmune condition caused by sensitivity to the protein gluten
57
Coeliac Disease: S+S
- Chronic or intermittent diarrhoea - FTT/faltering growth (in children)/weight loss - nausea and vomiting - fatigue - recurrent abdominal pain, cramping or distension - Anaemia
58
Coeliac Disease: Investigations
Serology: eat 6 weeks of gluten - Total IgA + IgA TTG antibodies - IgA endomysial antibodies (can lead to false positive above due to IgA deficiency) - anti-gliadin antibodies Duodenal Endoscopy + Biopsy: (gold) - villous atrophy - crypt hyperplasia - intraepithelial lymphocytes - lamina propria infiltration with lymphocytes
59
Coeliac Disease: Management
Gluten-free diet Immunisation: - Patients with coeliac disease might have functional hyposplenism - For this reason, all coeliac disease patients offered the pneumococcal vaccine + booster every 5 years
60
Irritable Bowel Syndrome: RF, S+S, Investigations
RF: depression, anxiety, female, lifestyle, 30 yrs Suspect if 6 months: ABC - Abdominal pain, and/or - Bloating, and/or - Change in bowel habit Diagnosis if: - Abdominal pain relieved by defecation/associated with altered bowel frequency stool form PLUS at least 2 of 4: 1. altered stool passage (straining, urgency, incomplete evacuation) 2. abdominal bloating (more common in women than men), distension, tension or hardness 3. symptoms made worse by eating 4. passage of mucus Red flags: - rectal bleeding - unexplained/unintentional weight loss - FH of bowel or ovarian cancer - > 60yrs Investigations: FBC, ESR/CRP coeliac disease: anti TTG
61
Irritable Bowel Syndrome: Management
1st line medical tx depends on predominant sx: - pain: antispasmodic agents - constipation: laxatives but avoid lactulose - diarrhoea: anti-mobility, loperamide 2nd line: - TCA - CBT Dietary advice: - regular meals, don't skip meals, long gaps between - 8 cups of fluid per day - restrict caffeine, alcohol, fizzy drinks - limit high-fibre food (eg. wholemeal, brown rice) - limit processed food starch - limit fresh fruit to 3 portions per day - for diarrhoea, avoid sorbitol - for wind and bloating: increase oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day).
62
Heart Failure: Types
inability of heart to deliver blood at a rate that is commensurate with requirements of metabolising tissues reduced cardiac output that results from a functional or structural abnormality De-novo HF: caused by increased cardiac filling pressures and myocardial dysfunction - Ischaemia: reduced cardiac output and therefore hypoperfusion, can cause pulmonary oedema - Viral myopathy - Toxins - Valve dysfunction Decompensated HF: (majority) - Acute coronary syndrome - Hypertensive crisis - Acute arrhythmia - Valvular disease
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Heart Failure: S+S
Symptoms - dyspnoea/orthopnoea: paroxysmal nocturnal dyspnoea - reduced exercise tolerance - oedema: ascites - fatigue - cough: worse at night, pink/frothy sputum - weight loss ('cardiac cachexia') Signs - Cyanosis - Tachycardia - Displaced apex beat - Bibasal crackles/cardiac wheeze - S3-heart sound - signs of right-sided heart failure: raised JVP, ankle oedema and hepatomegaly
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Heart Failure: Investigations
B-type natriuretic peptide: >400 = high → specialist + TTE in 2 weeks 100-400 = raised → specialist + TTE in 2 weeks Bloods - Underlying abnormality: anaemia, abnormal electrolytes or infection Chest X-ray - Alveolar Oedema - Kerley B lines: thickened septa - Cardiomegaly - Dilated upper lobe vessels of lung - Effusions (pleural) Transthoracic Echocardiogram - especially if cardiogenic shock or suspected valvular problems - can identify post-MI complications - ejection fraction <40%= HF with reduced ejection fraction: systolic dysfunction more likely
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Heart Failure: Acute Management
Acute: pour SOD - Pour away IV fluids + give nitrates (CI: hypotension) - Sit up - O2: 94-98% - Diuretics: loop: furosemide Treating Acute Hypotension - NO diuretics! can make it worse - Inotropic agents: dobutamine - Vasopressor agents: norepinephrine - mechanical circulatory assistance: intra-aortic balloon counterpulsation or ventricular assist devices
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Heart Failure: Chronic Management
1st line: - ACE-i +BB - Generally, one drug should be started at a time, choose, but need BOTH 2nd line: - Aldosterone antagonist, eg. spironolactone - monitor for SE hyperkalaemia - ACE and AA trigger Additional: - SGLT-2 inhibitors (for reduced ejection fraction) - Ivabradine - Hydralazine - Digoxin - Cardiac resynchronisation therapy - Annual influenza + pneumococcal vaccine
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Infective Endocarditis: Risk Factors
RF: - Previous episode of endocarditis (strongest) - valvular disease: mitral valve most common - prosthetic valves - congenital heart defects - IVDU - poor dental hygiene - immunocompromised/sepsis
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Infective Endocarditis: Causes
Causes - Staphylococcus aureus (most common) - Streptococcus viridans: linked with dental - Staphylococcus epidermidis: proesthetic valve - Streptococcus bovis: associated with colorectal cancer - non-infective: SLE (Libman-Sacks), malignancy (marantic endocarditis) Poor prognostic factors - Staphylococcus aureus infection - Prosthetic valve surgery - Culture negative endocarditis - Low complement levels Indications for surgery - severe valvular incompetence - aortic abscess (often indicated by a lengthening PR interval) - infections resistant to antibiotics/fungal infections - cardiac failure refractory to standard medical treatment - recurrent emboli after antibiotic therapy
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Infective Endocarditis: Investigations
2M/1M+3m/5m OR pathological obtained in surgery/autopsy (TEE is gold standard) Major Criteria (M) 1. Positive blood cultures: 2 positive cultures showing typical organisms 2. Evidence of endocardial involvement: positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or new valvular regurgitation Minor criteria (m) - predisposing heart condition or IVDU - fever > 38ºC - vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura - immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots
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Rheumatic Fever: Pathophysiology
Rheumatic fever develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection. Pathogenesis - Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells - B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated - there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry - the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries - this response leads to the clinical features of rheumatic fever - Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
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Rheumatic Fever: Investigations
Diagnostic criteria - recent strep infection AND 2M/1M+2m Major criteria: - erythema marginatum - Sydenham's chorea: this is often a late feature - polyarthritis - carditis and valvulitis (eg, pancarditis) - subcutaneous nodules Minor criteria - raised ESR or CRP - pyrexia - arthralgia - prolonged PR interval
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Rheumatic Fever: Management
1st: NSAIDs Antibiotics: oral penicillin V
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Hyperthyroidism: Causes
1. Graves' disease (TSH low, T4 high) most common cause of thyrotoxicosis as well as typically features of thyrotoxicosis other features may be seen including thyroid eye disease 2. Toxic multinodular goitre autonomously functioning thyroid nodules that secrete excess thyroid hormones 3. Drugs amiodarone
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Hyperthyroidism: S+S
Graves ophthalmopathy: - inflammation + swelling of extraocular muscles - photophobia, diplopia, decreased acuity - protruding eyes - corneal ulceration Graves dermopathy: - pretibial myxedema (raised purple skin lesions), - thyroid acropachy (clubbing, swollen fingers, periosteal bone) Other symptoms (general hyperthyroidism) - palpitations, increased HR, sweat - diarrhoea - weight loss despite increased appetite - fatigue - carpel tunnel syndrome - hyperkinesis (muscle spasms) - diffuse goitre - in children: excessive height/growth
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Hypothyroidism: Causes
-Primary hypothyroidism: problem with the thyroid gland itself, eg. an autoimmune disorder affecting thyroid tissue - Secondary hypothyroidism: due to a disorder with the pituitary gland or lesion compressing pituitary gland - Congenital hypothyroidism: thyroid dysgenesis/ dyshormonogenesis CAUSES: 1. Hashimoto's thyroiditis (TSH high, T4 low) - most common cause in the developed world, females - autoimmune disease, associated with T1DM, Addison's, pernicious anaemia Subacute thyroiditis (de Quervain's) associated with a painful goitre and raised ESR 2. Riedel thyroiditis - fibrous tissue replacing the normal thyroid parenchyma - causes a painless goitre 3. Postpartum thyroiditis 4. Drugs lithium amiodarone 5. Iodine deficiency the most common cause of hypothyroidism in the developing world
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Hypothyroidism: S+S
BRADYCARDIC: - Bradycardia - Reduced reflexes - Ataxia - Dry skin/hair - Yawn/drowsy - Cold - Ascites, oedema - Round puffy face - Depressed - Immobile, ileus - Congestive cardiac failure
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Hyperthyroidism + Hypothyroidism: Investigations
TSH + T4 levels Graves: TSH low, T4 high Hashimotos: TSH high, T4 low Antibodies - Anti-thyroid peroxidase (anti-TPO) antibodies - TSH receptor antibodies (more specific to Graves) - Thyroglobulin antibodies (more specific to Hashimotos) Other tests: - nuclear scintigraphy, toxic multinodular goitre reveals patchy uptake
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Hyperthyroidism + Hypothyroidism: Management
Hyperthyroidism: - Propanolol - Carbimazole - Propylthiouracil - Radioactive Iodine Hypothyroidism - levothyroxine (T4)
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Thyroid problems in Pregnancy
Untreated thyrotoxicosis increases the risk of fetal loss, maternal heart failure and premature labour Graves' disease is the most common cause of thyrotoxicosis in pregnancy. It is also recognised that activation of the TSH receptor by HCG may also occur - often termed transient gestational hyperthyroidism. HCG levels will fall in the second and third trimester Hyperthyroidism - Propylthiouracil is drug of choice (but associated with an increased risk of severe hepatic injury) - NO Carbimazole! Congenital abnormalities - Maternal free thyroxine levels should be kept in the upper third of the normal reference range to avoid fetal hypothyroidism Hypothyroidism: - levothyroxine is safe, increased dose needed in pregnancy, breastfeeding safe - TSH measured in each trimester and 6-8 weeks post-partum - women require an increased dose of thyroxine during pregnancy
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Post partum thyroiditis
Three stages 1. Thyrotoxicosis 2. Hypothyroidism 3. Normal thyroid function (but high recurrence rate in future pregnancies) Thyroid peroxidase antibodies are found in 90% of patients Management: thyrotoxic phase propranolol is typically used for symptom control not usually treated with anti-thyroid drugs as the thyroid is not overactive. hypothyroid phase usually treated with thyroxine
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Neonatal Hypoglycaemia
- Normal term babies can have hypoglycaemia in first 24 hrs of life but no harm as can use alternate sources like ketones and lactate - <2.6 generally considered hypoglycaemia Persistent/severe hypoglycaemia may be caused by: - Preterm - maternal DM - IUGR - hypothermia - neonatal sepsis - inborn errors of metabolism - nesidioblastosis - Beckwith-Wiedemann syndrome S+S: may be asymptomatic 1. Autonomic (hypoglycaemia → changes in neural sympathetic discharge) - 'jitteriness', irritable - tachypnoea - pallor 2. Neuroglycopenic - poor feeding/sucking - weak cry, drowsy - hypotonia - seizures 3. Others - apnoea - hypothermia Management: - Asymptomatic=encourage normal feeding + monitor blood glucose - Symptomatic/very low blood glucose: admit to the neonatal unit + IV 10% dextrose
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Group B Streptococcus Infection Pregnancy
Risk factors for Group B Streptococcus (GBS) infection: - prematurity - prolonged rupture of the membranes - previous sibling GBS infection - maternal pyrexia e.g. secondary to chorioamnionitis Screening: - screening should NOT be offered to all women - a maternal request is NOT an indication for screening - Women with previous GBS in pregnancy has 50% recurrence + should be offered intrapartum antibiotic prophylaxis benzylpenicillin (IAP) OR testing in late pregnancy and then antibiotics if still positive - Swabs for GBS at 35-37 weeks or 3-5 weeks before delivery date - IAP should be offered: previous GBS pregnancy, preterm labour (regardless of GBS status), >38ºC during labour
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Rubella Infection in Pregnancy
- most at risk in first 16w - classic features: cataract, deafness, cardiac abnormality - other possible features: jaundice, hepatosplenomegaly, microcephaly, reduced IQ
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Foetal Varicella Syndrome
- 1% foetuses affected if mother has primary infection in weeks 3-28 due to deactivation in utero - features: skin scarring, eye defects (small eyes, cataracts, chorioretinitis), neuro defects (reduced IQ, abnormal sphincter function, microcephaly)
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Maternal Syphilis Infection:
- Rhinitis, saddle-shaped nose, deafness (sensorineural hearing loss), Hutchinson's incisors - Hepatosplenomegaly, lymphadenopathy, anaemia, jaundice
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Prolactinoma
A type of pituitary adenoma: benign tumour of the pituitary gland. S+S Excess prolactin in women - amenorrhoea - infertility - galactorrhoea - osteoporosis Excess prolactin in men - impotence - loss of libido - galactorrhoea Other symptoms may be seen with macroadenomas - headache - visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia) - symptoms and signs of hypopituitarism Investigations: - MRI Management - Dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland - Trans-sphenoidal approach is generally preferred unless there is a significant extra-pituitary extension
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Urinary Tract Calculi: RF
RF: - dehydration - hypercalciuria, hyperparathyroidism, hypercalcaemia - cystinuria - high dietary oxalate - renal tubular acidosis - medullary sponge kidney, polycystic kidney disease - beryllium or cadmium exposure Risk factors: urate stones - gout - ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid Drug causes - drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline - thiazides can prevent calcium stones (increase distal tubular calcium resorption)
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Urinary Tract Calculi/Renal Stones: Types
Calcium Oxalate: - Hypercalciuria + Hyperoxaluria (diet, increased absorption, hyperparathyroidism) - Hypocitraturia: citrate forms complexes with Ca, makes it more soluble - Radio-opaque ( but less than Ca phosphate stones) Calcium Phosphate: - Renal tubular acidosis, high urinary pH increases supersaturation of urine with calcium and phosphate - Radio-opaque stones (composition similar to bone) Cystine: - Autosomal recessive: transmembrane cystine transport disorder leading to decreased absorption of cystine from intestine and renal tubule - Radio-opaque, yellow/pink Uric acid : - Uric acid is a product of purine metabolism - May precipitate when urinary pH low - May be caused by diseases with extensive tissue breakdown e.g. malignancy, associated with gout - More common in children with inborn errors of metabolism - Radiolucent Struvite - Stones formed from magnesium, ammonium and phosphate - Occur as a result of urease producing bacteria (and are thus associated with chronic infections) - Under the alkaline conditions produced, the crystals can precipitate - Slightly radio-opaque
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Urinary Tract Calculi/Renal Stones: S+S, Investigations
S+S: - loin pain: severe, intermittent 'colic' pain "loin to groin" - n+B - haematuria - dysuria - secondary infection may cause fever Investigations: - Non-contrast CT KUB should be performed on all patients within 24 hours admission - Ultrasound should be used for pregnant women and children - Urine dipstick and Culture - U+E - FBC, CRP - calcium/urate (cause) - Clotting if percutaneous intervention planned - Blood cultures if pyrexial or other signs of sepsis
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Urinary Tract Calculi/Renal Stones: Management
Renal stones - < 5mm and asymptomatic: watchful waiting - 5-10mm: shockwave lithotripsy - 10-20 mm: shockwave lithotripsy OR ureteroscopy - > 20 mm: percutaneous nephrolithotomy Uretic stones - shockwave lithotripsy +/- alpha blockers>< 10mm shockwave lithotripsy +/- alpha blockers - 10-20 mm ureteroscopy + strong analgesia (IV paracetamol/diclofenac, SE: Cardiac harm)
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Heart Block
Types of Heart Block First degree: consistently prolonged PR Second degree (Mobitz 1): inconsistently very prolonged or missing PR Second degree (Mobitz 2): consistently dropped QRS Third degree: no patterns at all Treatment: atropine for the bradycardia
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Acne Vulgaris: Pathophysiology
Comedones are due to a dilated sebaceous follicle - if the top is closed a whitehead is seen - if the top opens a blackhead forms Pathophysiology: - Follicular epidermal hyperproliferation resulting in the formation of a keratin plug - This causes obstruction of the pilosebaceous follicle. Activity in sebaceous glands may be controlled by androgen - Colonisation by the anaerobic bacterium Propionibacterium acnes leads to inflammation - In contrast, drug-induced acne is often monomorphic (e.g. pustules are characteristically seen in steroid use) - Acne fulminans is severe acne associated with systemic sx (e.g. fever). Hospital admission required and responds to oral steroids
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Acne Vulgaris: Staging
- Mild: open and closed comedones with or without sparse inflammatory lesions - Moderate acne: widespread non-inflammatory lesions and numerous papules and pustules - Severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring
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Acne Vulgaris: Management
Mild to moderate acne: -1st: 12-week course of topical combination therapy: either - topical adapalene + topical benzoyl peroxide - topical benzoyl peroxide + topical clindamycin - topical tretinoin + topical clindamycin benzoyl peroxide can be used as monotherapy if prefer no retinoid/antibiotics Moderate to severe acne: - 12-week course of one of the following options: - same as above or - topical adapalene + topical benzoyl peroxide + oral lymecycline/oral doxycycline - topical azelaic acid + oral lymecycline/oral doxycycline Important notes: - Gram-negative folliculitis may occur as a complication of long-term antibiotic use - high-dose oral trimethoprim to treat it - COCP is an alternative to oral antibiotics in women - oral isotretinoin: under supervision
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Acne Vulgaris: Antibiotic Resistance
DO NOT DO: - monotherapy with a topical antibiotic - monotherapy with an oral antibiotic - a combination of a topical antibiotic and an oral antibiotic Refer to dermatologist if: - patients with acne conglobata acne: rare and severe form, presents with extensive inflammatory papules, suppurative nodules (that may coalesce to form sinuses) and cysts on the trunk - patients with nodulo-cystic acne Consider referall if: - mild to moderate acne not responded to 2 treatments - moderate to severe acne not responded to oral antibiotic - acne with scarring/persistent pigmentary changes - acne is causing psychological distress
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Haemorrhoids
- Haemorrhoidal tissue is part of the normal anatomy which contributes to anal continence, made of mucosal vascular cushions - Haemorrhoids are said to exist when they become enlarged, congested and symptomatic S+S: - painless rectal bleeding is the most common symptom - pruritus - pain: usually not significant unless piles are thrombosed - soiling may occur with 3rd or 4th degree piles Types - External: originate below the dentate line, prone to thrombosis, may be painful - Internal: originate above the dentate line, do not generally cause pain Grade II → Prolapse on defecation but reduce spontaneously Grade III → Can be manually reduced Grade IV → Cannot be reduced Management - soften stools: fibre and fluid - topical local anaesthetics and steroids - outpatient tx: rubber band ligation or injection sclerotherapy - surgery for large symptomatic haemorrhoids - other tx: Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy - thrombosed haemorrhoid (purple, oedematous, tender lump) refer for excision
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Instrumental Delivery
when forceps or ventouse suction cup are used to help deliver baby, less common in women who've had a spontaneous vaginal birth before if assisted birth < 36w, forceps preferred over ventouse: less likely to damage baby's head, which is softer pre term Possible reasons: - You have been advised not to try to push out your baby because of an underlying health condition (such as having very high blood pressure) - abnormal baby's heart rate/fetal distress - breech/lie - premature baby - you require an epidural for pain relief during labour Risks of instrumental delivery: - Vaginal tearing or episiotomy - 3rd or 4th degree vaginal tear - Higher risk of blood clots - Urinary/Anal incontinence
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Obstructed Labour
Labour that does not advance despite adequate uterine contractions: - Cephalo-pelvic disproportion: A mismatch between the size of the baby's head and the mother's pelvis - Malpresentation: The baby is positioned in a way that makes it difficult to pass through the birth canal, such as a brow or shoulder presentation - Contracted pelvis: The mother's pelvis is smaller than normal, which can be caused by malnutrition
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Hypoactive Uterus
WHO defines uterine hypoactivity as having two or fewer contractions in 10 minutes, each lasting less than 40 seconds. - Can be caused by overdistension of the uterus, or by the fetus being malpositioned. - Contractions can be strengthened through rehydration, relaxation, and the use of intravenous syntocinon
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Constipation in Adults
Defined as defecation that is unsatisfactory because of infrequent stools (< 3 times weekly), difficult stool passage (with straining or discomfort), or seemingly incomplete defecation. Management - investigate and exclude any secondary causes+ red flags - Exclude faecal impaction - Lifestyle: fibre, fluids, activity levels - 1st line laxative: bulk-forming laxative first-line, such as ispaghula - 2nd-line: osmotic laxative, such as a macrogol Complications - overflow diarrhoea - acute urinary retention - haemorrhoids
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Constipation in Children
Most are idiopathic but others include: - dehydration, low-fibre diet, medications: e.g. Opiates, anal fissure, over-enthusiastic potty training, hypothyroidism, Hirschsprung's disease, hypercalcaemia, learning disabilities Management: - lifestyle + rule out red flags - 1st: polyethylene glycol 3350 + electrolytes (Movicol Paediatric Plain) using an escalating dose regimen as the first-line treatment - add a stimulant laxative if Movicol Paediatric Plain does not lead to disimpaction after 2 weeks - substitute a stimulant laxative singly or in combination with an osmotic laxative such as lactulose if Movicol Paediatric Plain is not tolerated - inform families that disimpaction treatment can initially increase symptoms of soiling and abdominal pain
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ECG Changes
- PE: sinus tachy, right axis deviation, RBBB, S1Q3T3 (S wave in lead 1, Q wave in lead 3 inverted T wave in lead 3) - Hyperkalaemia: Tall tented T waves, small P wave, wide QRS - Hypokalaemia: U wave, tall P wave, T wave flattening / inversion, long PR, ST depression - UA/NSTEMI: ST depression, inverted T wave - STEMI: ST elevation, tall T waves, LBBB, pathological Q - Acute pericarditis: Saddle-shaped ST elevation, PR depression - AF: absent p, irregular irregular
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GTN advice
- Contraindicated in severe aortic stenosis - Most common side effects are flushing, headaches, light headedness, and hypotension. Continued use of nitrates can lead to tolerance. To minimise tolerance, patients should take one dose in the morning and one mid afternoon to allow >12 hours between afternoon and subsequent dose in the next morning. - Sit down and rest before and for 5 minutes after taking GTN.
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Acute Pericarditis
Investigations 1. ECG 2. Troponin: raised 3. CXR: enlarged globular heart 4. Echo if suspected pericardial effusion 5. CMR/CT: localised inflammation 6. Viral serology, blood cultures, autoantibodies, TFT, 7. Other routine FBC ESR U&E Causes: TB, pneumonia, SLE, RA, Dressler, Isoniazid, Coxsackie, EBV, CMV, Trauma, Chronic heart failure, MI, Hypothyroidism, IBD, Amyloidosis, Uraemia Management: NSAIDs/Colcichine Cardiac tamponade Beck’s triad ● Muffled heart sounds ● Raised JVP ● Hypotension
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Atrial Fibrillation
ECG – irregularly irregular rhythm, absent p waves Management: - Unstable = DC Cardioversion + heparin - Stable = Propanolol – 1st line, Verapamil, amiodarone, digoxin
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MI
Treatment: BATMAN (BB), Aspirin, Ticagrelor/Clopidogrel, Morphine, Anticoagulants, Nitrates Starlings law: the stroke volume of the heart increases in response to an increase of blood filling the heart (the EDV). This is due to increased stretch of the LV wall which causes the cardiac muscle cell to contract more forcefully
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Pneumonia
Confusion (AMT ≤8) Urea >7mmol/L Respiratory rate ≥30/min BP <90 systolic and/or 60mmHg diastolic) Age ≥65 0-1 – antbiotics/home treatment 2 – hospital therapy ≥ 3 – severe pneumonia – consider ITU 1-2 – give PO amoxicillin + erythro 3-5 – IV amoxiclav + erythro
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Question on asthma + cardiac arrest
pulseless ECG, ● ABCDE- Secure airway – head tilt chin lift. ● Call resuscitation team ● Begin CPR 30:2 ● 100% O2 ● IV access – large bore cannula – fluids - Hartmann’s Immediate drug and route Adrenaline IV 1mg Heart came round what 4 things would you do now? - As per ALS resus guidelines - ABCDE Assessment again - ABG: aim for SpO2 94-98, normal PaCO2 - ECG - Treat precipitating cause - Intra arterial blood pressure monitoring - Speak to ITU, transfer to ITU/HDU, What 2 other rates are shockable - VF - PULSELESS VT Why would an asthmatic get these rhythms? Hypoxia
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TB: Treatment
Rifampicin: blocks protein synthesis, SE: red urine, hepatitis Isoniazid: blocks cell wall synthesis, SE: peripheral neuropathy, hepatitis (give with pyridoxine B6), hepatitis Pyrazinamide: bactericidal, SE: hepatitis, arthrlagia, rash Ethambutol: blocks cell wall synthesis, SE: optic neuritis R+I: 6 months P+E: first 2 months
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TB: Investigations
1. Sputum microscopy: Ziehl-Neelsen Stain for acid-fast bacilli 2. Sputum culture: Lowenstein Jensen sputum culture + sensitivity 3. Nucleic acid amplification test direct detection of M. tuberculosis in sputum by DNA or RNA amplification, this can also detect drug resistance
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Oral Anticoagulants
LMWH – dalteparin, enoxaparin, tinzaparin – inactivates factor Xa (but not thrombin) Unfractionated Heparin - binds to anti-thrombin, increasing its ability to inhibit thrombin, factor Xa and IXa Warfarin – inhibits reductase enzyme responsible for regenerating the active form of vitamin K, producing a state analogous to vitamin K deficiency. This inhibits the synthesis of vitamin K-dependent clotting factors, factor 2,7,9,10 When starting anticoagulants, start both LMWH and warfarin together, warfarin initially inhibits protein C and S also, which leads to a procoagulant state before inhibiting production of factors 2,7,9,10. LMWH is to cover during this procoagulant period. Stop heparin when INR 2-3 on 2 consecutive days.
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Homan sign
in DVT, Pain in the calf on dorsiflexion of the foot
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DKA
S+S - abdominal pain - polyuria, polydipsia, dehydration - Kussmaul respiration (deep hyperventilation) - Acetone-smelling breath ('pear drops' smell) - lethargy, anorexia, dehydration, coma Metabolic/Biochemical Abnormalities: - Metabolic acidosis (DM), ph <7.3, low bicarbonate <15 - Hyperglycaemia (DM) - Ketonaemia <0.6, ketonuria - Hyperkalaemia (absence of insulin which shifts potassium out of cells) but total might be low Management: 0.9% saline insulin
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Hypercalcaemia
- Renal stones - Bone pain - Depression - Abdo pain, nausea, constipation, anorexia, weight loss List 2 ways PTH works to increase serum calcium (location and effect)? 1. Increases osteoclast activity by releasing Ca2+ and PO4 3- from bones (bone resorption) 2. Increases calcium but decreases phosphate reabsorbtion from kidney (proximal convoluted tubule) 3. Increases active 1,25 dihydroxyvitamin D3 production by activating 1 alpha hydroxylase in kidney.
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Acromegaly
In acromegaly there is excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of cases are caused by ectopic GHRH or GH production by tumours e.g. pancreatic. Features - coarse facial appearance, spade-like hands, increase in shoe size - large tongue, prognathism, interdental spaces - excessive sweating and oily skin: caused by sweat gland hypertrophy - features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia (press on optic chiasm) - raised prolactin in 1/3 of cases → galactorrhoea - 6% of patients have MEN-1 Complications - hypertension - diabetes (>10%) - cardiomyopathy - colorectal cancer Investigations: - 1st: Serum IGF-1 levels: HIGH - 2nd (confirm if IGF-1 high): OGTT: NOT SUPPRESSED like normal person would Management: - 1st: Trans-sphenoidal surgery - If cannot do surgery: Ostreotide (somatostatin analogue, inhibits GH), Pegvisomant (GH receptor antagonist)
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Addisons Disease
Autoimmune destruction of the adrenal glands is the most common cause of primary hypoadrenalism= Addison's disease = low cortisol and aldosterone Other causes of hypoadrenalism: TB, metastases, meningitis, HIV, antiphospholipid syndrome S+S: - lethargy, weakness, anorexia, nausea & vomiting, weight loss, 'salt-craving' - hyperpigmentation (especially palmar creases) - vitiligo - loss of pubic hair in women - hypotension - hypoglycaemia - hyponatraemia and hyperkalaemia may be seen - crisis (extreme low cortisol, precipitated by infection, trauma, surgery): collapse, shock, pyrexia, tachy → hydrocortisone + saline dextrose Investigations: - Synacthen Test, might see 21-alpha hydroxylase antibodies - low: glucose, sodium - high: potassium, urea, creatinine, - metabolic acidosis Management: - Hydrocortisone: glucocorticoid fludrocortisone/mineralocorticoid - MedicAlert bracelets - steroid cards
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Diabetes Medication
Metformin (biguanide): - Increases insulin sensitivity. It reduces glucose production by the liver and sensitizes target tissues to insulin - Nausea, diarrhoea, abdominal pain, NOT hypoglycaemia - Avoid if renal failure due to lactic acidosis DPP4 inhibitors/gliptins (sitagliptin) - Blocks the action of DPP-4 an enzyme which destroys incretin Sulfonylurea (gliclazide) - Increases insulin secretion - SE: Hypoglycaemia (monitor glucose), weight gain, nausea, vomiting diarrhoea. Can cause hypersensitivity reactions and agranulocytosis SGLT-2 inhibitor (Empagliflozin) - Sodium-glucose co-transporter 2 inhibitor, this blocks reabsorption of glucose in the kidneys, and promotes excretion of glucose in the urine - SE: UTI, genital candida - good for CVD comorbidities Glucagon-like peptide analogies (Exenatide, liraglutide) - Promotion of insulin release, inhibition of glucagon release, prolongation of gastric emptying and a reduction in hunger - Patients must have BMI >35 or <35 and insulin therapy would have occupational implications mediated by receptors in the brain.
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2012 SAQ
Young woman with secondary amenorrhoea, galactorrhoea. MRI pituitary reveals tumour compressing optic chiasm. 1. Describe the visual field defect she will be likely to have (2) Bitemporal hemianopia 2. Explain why she has amenorrhoea. (2) Raised prolactin levels inhibit the secretion of gonadotropin releasing hormone in the hypothalamus. This inhibits the secretion of LH and FSH – hormones which regulate the menstrual cycle. This results in amenorrhoea 3. The prolactin is only modestly elevated and it’s determined that it’s not a prolactinoma. How can a nonfunctioning pituitary tumour cause elevated prolactin? (2) Compression of the pituitary stalk by the tumour reducing local dopamine levels. This results in uninhibited prolactin secretion. 4. TSH (normal) and free T4 (low) measurements given. What is the diagnosis and explanation? (2) Hypothyroidism – explanation TCB 5. She is found to be deficient in cortisol. What drug and route would you give before her pituitary surgery? (2) IV hydrocortisone
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Conns Question
3. Patient presented with confusion and hyperkalaemia, conn’s syndrome diagnosed (ECG given) What hormone level is elevated in conn’s? Which organ is it from? Aldosterone, zona glomerulosa of adrenal cortex in adrenal gland What hormone level is suppressed in conn’s? Which organ is it from? Renin – kidneys Name features on the ECG that is suggestive of hyperkalaemia Tall tented T waves, small P wave, wide QRS. Hypokalaemia U wave, tall P wave, T wave flattening / inversion, long PR, ST depression What is the first line image of choice in conn’s syndrome? CT adrenals Spironolactone: Where does it act in the nephron? Collecting duct What happens at the mineralocorticoid receptor site? Spironolactone displaces aldosterone from the mineralocorticoid receptor. What channel does mineralocorticoid act on? Epithelial sodium channels (ENaC)
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Drugs that potentially interfere with absorption of Levothyroxine:
Ferrous sulfate, calcium carbonate, PPIs, antacids
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CLL Where would you take biopsy from
posterior iliac crest
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Haemophilia A Findings
Bleeding time – Normal PT – normal VWF - Normal APTT – Increased VIII:C (Coagulant factor 8) - Decreased
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Beta Thalassemia Question:
3 month old baby boy from.....some Asian country. His weight is below 95th centile, he is pale and miserable. The diagnosis of β-thalassaemia major is made. Which investigation do you do to diagnose β-thalassaemia? - DNA analysis - Hb electrophoresis - FBC, blood film, skull XR What condition must both his parents have? Beta-thalassaemia minor If the child had been born in the UK, what 2 public health initiatives would have allowed his condition to be picked up earlier? Antenatal screening Neonatal blood spot test GP 6-8wk health check How do you treat β-thalassaemia major? - Life-long transfusion to keep Hb >90g/L to suppress extramedullary haematopoiesis and to allow normal growth. - Chelating agents deferiprone - Folic acid supplementation The treatment you give has complications. Name 3 organs that may be affected by the treatment you give, and the effect on the organs. - Iron deposition -> liver (cirrhosis), pancreas (DM), heart, thyroid-> hypothyroidism, pituitary (hypogonadism) How do you prevent these complications? Iron chelators deferiprone PO and desferrioxamine SC (SE: pain, deafness, cataracts, retinal damage, increased risk of Yersinia) (large doses of ascorbic acid can also help by increasing urinary excretion of iron) α-thalassaemia major is never seen in primary care. Why is that and what is the pathophysiology behind it? - incompatible with life, and babies are either stillborn or die shortly after birth (Bart’s hydrops). The pathophysiology is that mutations occur in all four of the alpha-globin genes, meaning that no alpha chains can be formed and so normal HbA cannot be produced. The baby thus develops severe fetal anaemia.
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Joint Pain question
Anaemia of 6.0, old lady with osteoarthritis, hypertension for 10 years. Is on diclofenac, atenolol and bendroflumethiazide. Resting heart rate is 54 regular. Description of blood results 1. Describe her anaemia (i.e. cell size, colour etc) 2. What drug most likely to cause this type of anaemia? Diclofenac (NSAID) 3. Mechanism by which this drug causes this anaemia Peptic ulcer subsequent bleeding 4. 4hrs after transfusion, a pyrexia of 38 degrees. Cause? Non-haemolytic febrile transfusion reaction. (1 unit of blood increases haemoglobin by 10-15g/L) (A temperature rise of 1°C or greater above baseline may indicate an acute haemolytic transfusion reaction due to blood group incompatibility and is an indication to stop the transfusion.) 5. List 3 other complications which may present within hours of a blood transfusion. Before 24 hours ● Anaphylaxis ● Fluid overload ● Acute haemolytic reactions (ABO or Rh incompatibility) ● Infections ● Iron overload ● Post transfusion purpura – potentially lethal fall in platelet count 5-7days post transfusion requiring treatment with IV immunoglobulin and platelet transfusion 6. NSAIDs may interact with one of the drugs she is taking. How and what would his cause. Atenolol – NSAIDs reduce the therapeutic effect of antihypertensives and diuretics. 7. Why is her potassium low? Diuretics
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Medications that cause postural hypotension
- nitrates - diuretics - anticholinergics - antidepressants - beta-blockers - L-dopa - ACEi
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Medications associated with falls due to other mechanisms
- benzodiazepines/sedating agent - antipsychotics - opiates - anticonvulsant - codeine - digoxin
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Fall risk factors
Previous fall Lower limb muscle weakness Vision problems Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson's disease etc) Polypharmacy (4+ medications) Incontinence >65 Have a fear of falling Depression Postural hypotension Arthritis in lower limbs Psychoactive drugs Cognitive impairment
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Breastfeeding Benefits
Infant Benefits: - Less Infection - Less immune driven/allergic disease: - Reduces risk of NEC
 - Reduced SIDS
 - Reduced Gastroesophageal Reflux
 - Lower risk of Childhood Inguinal Hernia
 - Higher IQ
 - Better Cognitive Development Maternal Benefits: - Reduces cancer risk: Breast, Uterine, Ovarian, Endometrial - Reduces: PPH, postnatal depression, osteoporosis, insulin requirements in diabetics, - Less child abuse - Promotes postpartum weight loss - Less food/medical expense, more ecological
 - Delays fertility
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Vomiting receptors
muscarinic (M1), dopaminergic (D2), histaminergic (H1), 5-hydroxytriptamine or 5-HT3  (serotonin), neurokinin NK1  (substance P) Precipitants: - toxic material in the lumen of the GI tract  - visceral pathology  - vestibular disturbance  - central nervous system stimulation  - toxins in the blood or cerebrospinal fluid (CSF).