GP Flashcards
What are some of the causes of secondary hypertension?
Chronic Renal disease (Polycystic kidneys, diabetic glomerulosclerosis, glomerulonephritis)
Vascular - Renal artery stenosis and coarctation of aorta
Endocrine - Adrenal tumours secreting aldosterone, cortisol, ACTH, catecholamines (pheochromocytoma); cushing’s
Sleep apnoea
Meds (steroids, high oestrogen states such as OCP, HRT, pregnancy)
NOT atherosclerosis (except in case of renal artery stenosis)
How is the treatment protocol (pharm vs lifestyle modification) for different categories for HTN divided up?
Stage 1 SBP 140-179 ; DBP 90-109 with NO CV RFs: life style modification (pharm treatment if still high after 6 months)
Stage 1 SBP 140-179 ; DBP 90-109 WITH CV RFs or end-organ damage: start pharmacological treatment
Severe HTN SBP>180 ; DBP>110: start pharmacological treatment
Pharm. treatment (order of use) for HTN
Step 1:
If <55yo, ACE inhibitor (or AT1Rantag)
If >55yo or afro-carribbean origin - Ca channel blocker
if >65yo - low dose thiazide
Step 2:
ACE inhibitor + Ca channel blocker
Step 3:
Add thiazide diuretic (or beta blocker only if patient has IHD and heart failure)
If BP still elevated after step 3 = RESISTANT HTN
Step 4: Refer. Consider further diuretic (thiazide-like or spironolactone) or beta or alpha blocker
What drug combinations to avoid in HTN and why? (3)
- Ace inhibitor + K-sparing diuretic (spironolactone) - risk of hyperkalaemia
- Ca channel blocker + beta blocker - risk of heart block
- ACEi + AT1R antag - not shown to be clinically effective
LONG-TERM Treatment protocol for CHF
- Lifestyle modification
Smoking and alcohol cessation
Na and fluid restriction
Diet and exercise (weight control) - Treat underlying cause and aggravating factors (valvular disease/arrhythmia; thyroid, infection, anaemia, HTN)
- Meds
ACE inhibitor/ARB (slows progression, improves survival)
+ Beta blocker (slows progression, improves survival)
+/- aldosterone antag*(spironolactone) if severe and symptomatic
+/- diuretic (furosemide) if fluid overloaded
+/- digoxin (SX control only)
+/- antiarrhythmic (if AF)
+/- Warfarin (if AF, prior TE or LV thrombus on echo)
*mortality benefit
Precipitants/exacerbaters of heart failure
MADHATTER: MI/ischaemia Anaemia Drugs (NSAIDs, steroids, non-compliance) HTN Arrhythmias Thyroid Toxic (infection) Endocarditis/embolus Renal failure
Stable angina vs unstable angina
Stable:
- pain comes on w exercise, cold, stress and is relieved by stress. REPRODUCIBLE.
- due to atherosclerotic narrowing
Unstable:
- new onset pain or pain at rest
- accelerating pattern of pain
- pain post MI or post-procedure
- due to acute plaque event (plaque rupture, acute thrombus formation, partially occludes vessel)
STEMI vs non-STEMI
STEMI: Criteria for MI + ST elevation or new BBB
NON-STEMI: Criteria for MI WITHOUT ST elevation or new BBB
Criteria for MI
2 of the following:
- Classic SX of MI
- Elevated troponin, CK
- Typical ECG pattern (ST segment changes, T wave changes, new BBB, development of Q waves)
Long-term management of IHD post-acute ACS event (8)
- Dual anti-platelets (aspirin + clopidogrel)
- Beta blockers (Ca channel blocker second line)
- ACE inhibitors (prevent remodelling)
- Nitrates (GTN) PRN for symptom relief
- Statin (irrespective of cholesterol levels for plaque stabilisation)
- Modify lifestyle (exercise, diet, cease smoking, weight control, alcohol, stress)
- Modify CV Risk Factors (diabetes, cholesterol, HTN)
- Review (1 month then 6 mo thereafter)
Standard Management of dyslipidaemia
Manage modifiable risk factors
- Smoking cessation
- Diet (reduce saturated fats and refined sugars, incr fruit veg and fibre)
- Reduce alcohol
- 150min mod-intense exercise/week
- Weight reduction
Medications
- Statins are 1st line mono therapy
- If severe, add Fibrates +/- fish oil
Monitoring
- Monitor LFTs and CK at baseline then 6 weeks after starting statin (SEs)
- Fasting lipids at 3 mo, and if under control, monitor every 6-12 months thereafter.
What is the screening protocol for hyperlipidameia?
Full fasting lipid profile every 3 years for
○ Males > 40
○ Females > 50 (or menopausal)
○ Anyone with other CAD risk factors
Risk factors for AF
CHADS2
CCF HTN Age >75 DM Stroke/TIA/Thromboembolus previously
Management of CHRONIC AF
- Evaluate stroke risk and manage -> score 0 gets aspirin; score >1 gets anticoagulation (warfarin or NOAC)
- Rate control if patient stable (beta blocker, diltiazem, verapamil or digoxin, or amiodarone last line)
Rhythm control (SOTOLOL. flecainide»_space;> amiodarone if in HF) if patient is symptomatic or younger or has CCF
Triggers of AF
Heart failure/ischaemia HTN MI PE Valvular disease (mitral) Hyperthyroid Caffeine/alcohol
Management of Acute AF (<48 hours)
If very ill or haemodynamically unstable:
- O2
- Emergency cardioversion (electrical or IV amiodarone if unavailable. Flecanide)
- Rate control (Verapamil or Bisoprolol = Ca channel or beta blocker; digoxin or amiodarone 2nd line)
- Anticoagulation (LMWH)
Treat any triggering illnesses (pneumonia, MI, PE etc)
Sx and signs of PAD?
SX:
Claudication
Rest pain
Signs: Rubor Ulcers, gangrene, cellulitis Abnormal nails Shiny, hairless, cool/pale Decr pulses
Management of intermittent claudication
Lifestyle modification w intermittent claudication:
○ Diet and lifestyle
○ BP control (ACEi)
○ Aspirin
○ Statins
○ Smoking cessation
○ Exercise (improves fitness and general pump function as well as efficiency with using O2 delivered (if they stop walking to ‘control symptoms’ they will lose their legs)
Surgical mx w rest pain:
§ End-arterectomy for short segments
§ Angioplasty and stenting for short segments
§ Bypass for longer blocks
§ Amputation or palliation if unfit for surgery
Clinical presentation of chronic venous disease
Hyperpigmentation and haemosiderin staining
Brawny pitting OEDEMA
Lipodermatosclerosis
Varicose veins
Ulcers
Leg heaviness, ache and fatigue at end of day
Venous eczema: Pruritis, pain, swelling, erythema, recurrent cellulitis
LEg elevation, compression alleviates pain
What is venous disease caused by?
Venous HTN and venous insufficiency
causes of venous HTN (=OLD AGE)
- inadequate muscle pump function
- incompetent venous valves -> reflux
- venous thrombus or obstruction
Venous HTN leads to vein dilatation, skin changes and or ulceration
Treatment of peripheral venous disease
Initial conservative
§ Leg elevation - improves O2 delivery and reduces oedema
§ Compression - compresses dilated veins and reduces oedema; helps heal ulcers
§ Exercise - improves O2 delivery
§ Topical dermatological agents for stasis dermatitis
Vein ablation - surgical excision, sclerotherapy, thermal ablation
§ Requires a minimum of 3 months conservative therapy before proceeding w ablation.
Venous reconstruction (translocation of vein segments, transplantation of vein segments, substitution)
Treatment varicose veins
Compression stockings Leg elevation Injection sclerotherapy Surgery - vein removal (Stripping, ligation) Vein ablation
Characteristics of venous ulcers
Commonly found in gaiter region - medial aspect of calf/ankle
Large, flat/shallow
Irregular edges
Granulomatous base (pink/beefy red)
Mild pain
Pedal pulses present
Characteristics of arterial ulcers
VERY PAINFUL
Often on foot pressure point areas
Small size
Deep with punched out appearance
Regular margins
Sloughy/necrotic base
Absent pedal pulses
Neuropathic ulcer characteristics
Often very large but size and shape varies
NOT PAINFUL
Appearance: Prominent hypertrophied squamous rind around edge
Often on feet -pressure point areas
ECG anomalies assoc w syncope
Sinus bradycardia
Conduction block
Wolff Parkinson white syndrome
How to intensify the MR and AS murmurs
MR: get patients to roll onto L side and inspire
AS: Patient leans forwards and expires
Signs of RHF vs LFH
RHF: incr JVP, hepatosplenomegaly, ascites, peripheral oedema
LHF: pulmonary oedema -> lung crackles (SX: SOB, orthopnoea, PND)
Complications of HTN
Renal:
Diabetic glomerulosclerosis
Polycystic kidneys
Glomerulonephritis
Vasc:
- Worsens Arteriosclerosis
- Worsens Atherosclerosis -> aneurism / dissection
- Hyaline arteriolosclerosis
- Berry aneurysm
- Acute plaque event -> thrombus formation, thromboembolism
Cardiac
- IHD and infarct
- LV concentric hypertrophy
- Cardiac failure
Kidney
- Benign nephrosclerosis (elevated BP transmitted to glomeruli which respond with tubular fibrosis, sclerosis and atrophy & hyaline arteriolosclerosis -> kidney ischaemia)
Brain
- Ischaemic Strokes (atherosclerotic TE)
- Haemmhoragic stroke (due to hyaline arteriolosclerosis in basal ganglia or SA haemmhorage due to ruptured berry aneurysm)
Eye complications of HTN
- Hypertensive retinopathy
- (hyalinised retinal vessels are weak and leaky, can bleed or lead to ischaemia).
Treatment rosacea
No cure - avoid triggers (sunlight, hot or spicy foods, heat, alcohol, topical steroids)
Makeup, moisturiser, sunscreen
Topical Abx: Metronidazole
Systemic doxyclycine or systemic retinoids if inflammatory ethology
Vascular laser if vascular etiology
Ablative laser if rhinopehyma
TOPICAL STEROIDS MAKE THINGS WORSE!
Characteristics of rosacea
How is this different from acne?
Tendency to flush/blush
+/- burning sensation
Florid ruddy complexion all the time - affecting convexities of face
+ Papules, pustules
Telangiectasia
Worse w vasodilation, wind, stress etc
Doens’t have comedones, unlike acne
Contact dermatitis - compare the 2 types
Irritant (non-immune) - redness, dry skin, fine scale, burning
- commonly due to nickel in belt buckles
Allergic (t4 hypersensitivity) - vesicular, redness, swelling, itchy .
- usually flexor surfaces
- commonly due to poison ivy.
Eczema vs Psoriasis
Signs
Eczema: flexor
Acute - weepy, crusting, red, blistered lesions. diffuse.
Chronic - dry thickened, scaly and itchy lesions
Psoriasis: extensor
Salmon pink erythematous plaques, with silvery scales
Eczema treatment
chronic vs acute flare
E:
Prevention:
- avoid triggers (extremes of temp, dry/extreme heat, soap and detergents)
- regular emollients
- warm/cool (soap-free) baths, wet compress
- if above doesn’t work, can try low dose topical steroid
Acute flare:
- 1st line - Potent topical steroids (mild ones for face)
- 2nd line - Topical calcineurin inhibitors (Elidel; ok for face)
- Topical/oral abx if suspect bacterial infection (golden crusty)
- Twice weekly bleach baths if recurrent infections
Severe: oral steroids or immunosuppressants (methotrexate, azathioprine etc)
1-2 weeks after strep URTI.
Guttate psoriasis. (small plaque psoriasis, almost looks like red mosquito bites)
Which type of psoriasis is associated w strep pharyngitis (strep throught)?
BCC characteristics
Pearly/transulent firm nodule
Rolled edges
+/- central indentation or ulceration (“rodent ulcers”)
Telangiectic border (red) painless bleeding
Indolent growth
SCC characteristics
Erythematous nodule or plaque
Hyperkeratotitic surface crust (keratinocyte proliferation)
Ulceration, bleeding
Grows quickly, over weeks-months
May be tender to palpation
SCC
- level of invasion
- where are they found?
- More likely to spread than BCC (to regional lymph nodes first)
- Sun exposed sites
Management of SCC
COMPLETE wide local excision with biopsy +/- adj. radiotherapy
Not for surgery: radiotherapy alone
lifelong follow up
Descibring skin lesions ABCDE
Asymmetry Borders (irregular) Colour (variated) Diameter (>6mm) Evolution
WHAT WOULD you use to characterise the prognosis of melanoma?
Breslow thickness - thickness of lesion based on biopsy histology determines recommended margin for wide local excision
What do you do about a suspicious lesion if they are:
- Raised
- Flat
- Pigmented/suspicious for melanoma
Raised: shave biopsy
Flat:
- Large: Punch biopsies of most suspicious areas
- Small: Wide excision if small
Pigmented/melanoma - complete wide excision
DX, investigations and treatment: itchy rash with a gradually enlarging red scaly edge and clearing central pale region
Tinea Corporis (ring worm)
- Fungal infection -> skin scraping for fungal MCS
- Treat with topical anti fungal cream (imidazole)
What is the significance of solar or actinic keratosis ?
What are red flags?
What do you do about them?
10% can develop to SCC
Watchful waiting
If suspicious for transformation to SCC (growing, hyperkeratotic, TENDER):
Cryotherapy
Topical medications (5-Fu, imiquimod)
Surgical excision
Actinic keratosis:
Where are they generally found and what are key features?
Found on sun exposed skin - face, scalp, forearms and hands
Scaly erythematous lesions, sand-papery texture +/- actinic horn
What is Bowen’s disease?
Appearance?
SX?
What is the significance of them?
Intraepithelial SCC (early non-invasive stage of SCC = full thickness epithelial dysplasia without breaching BM)
Appearance: perisistant red-brown scaly patch, NOT indurated
Location: sun exposed sites, particularly lower limbs!
SX: may be itchy/painful/bleed but often asymptomatic
Significance: 5% progress to invasive SCC.
Topical meds for removing skin lesions
5-fluorouracil cream
Imiquimod cream (IFN)
Photodynamic therapy
BCC
- level of invasion
- where are they found?
Local invasion (almost never metastasise)
Found on face
What causes warts?
Treatment of warts
HPV infection Destructive - liquid nitrogen - diathermy - curettage
Topical
- salicylic acid (keratolytics)
- DCP immunotherapy
- Imiquimod (genital warts)
- Tape
Impetigo: what is the generic name?
What organism causes impetigo and what is the characteristic appearance?
“School sores”
Staph aureus - treat w systemic flucloxaillin or cephalexin
Honey-comb crusting
Topical antibiotics such as mupirocin, fusidic acid, and retapamulin are the first-line treatment options
Oral flucloxacillin for widespread lesions w no systemic involvement.
IV if evidence of systemic involvement/cellulitis.
Treatment for psoriasis
Topical therapy
-steroids, topical vitD, keratinolytics
Emollients
UVB phototherapy
Systemic immunosuppressants and biologic agents
Sites where psoriasis is usually found
Extensor surfaces
Scalp
AnoGenital (more of a glazed appearance, less scaly)
palmar and plantar surfaces
Nails - psoriatic arthritis more likely with nail involvement
Auricular
Cellulitis: common causative agents
TX
Strep pneumonia! Otherwise staph aureus, staph epidermis.
Requires IV antibiotics (dicloxacillin, augmentin, cephalexin or vancomycin if MRSA suspected) and usually overnight admission due to systemic illness
Management acne
Mild disease: topical retinoid +/- topical Abx +/- BPO
OR salicylic acid
Moderate: oral ABx + BPO + topical retinoid. OR anti androgens (females only)
Conservative/general principles:
Avoid aggravators (humidity, cosmetics and oils to face, scratching or picking, lithium and steroids)
Diet - fresh fruit and veg, low protein, dairy and low GI diet (evidence weak)
Stop smoking
Sunlight
Topical (Creams)
- salicylic acid and retinoic acid (act to dissolve comedones)
- benzoyl peroxide
- abx (clindamycin, erythromycin)
Systemic (Oral)
- Antibiotics (doxy, erythromycin, minocycline)
- Anti-androgens (OCP, spironolactone, cyproterone acetate) for females w hormonal-type acne
- Systemic retinoids (roacutaine) - severe acne only. 60-70% Curative after one 6-12mo course.
Features of acne
Comedones (open are black heads and closed are white heads)
Papules (no pus), pustules (pus)
Nodular pseudocysts
Scarring
Hormonal - Onset in adolescence
Genetic
complications of rosacea
Rhinophyma (tissue hyperplasia of the nose)
Ocular Rosacea
◦ Occurs in 20-40% of cutaneous rosacea
◦ Symptoms: Grittiness, stinging, dryness, itching
◦ Signs: watery, bloodshot appearance
Telangiectasia (chronic rosacea -> permanent dilation of blood vessels)
DX, investigations and treatment
Small papule often between fingers with linear lesions on hands - VERY itchy, with itch worse at night.
Can spread to genitals in men or nipples in women.
Turns into generalised eczematous body rash as a late secondary hypersensitivity reaction.
Scabies
Skin scraping -> light microscopy
Treat w 5% permethrin cream + hot wash and dry of all clothes and beddings.
Treat ALL CONTACTS!
Treat accompanying eczema (topical steroids, emollients, oral antihistamines etc)
What virus causes shingles?
Herpes Zoster Virus - Varicella Zoster sits latent in DRG and reactivates when host is immunosuppressed or stressed and causes vesicular/papular crusty rash in dermotomal pattern.
May have prodrome of neuralgic pain and tingling
Diagnosis via PCR
Systemic antiviral treatment
DX, investigations and treatment: itchy rash with a gradually enlarging red scaly edge and clearing central pale region
Tinea Corporis (ring worm)
- Fungal infection -> skin scraping for fungal MCS
- Treat with topical anti fungal cream (imidazole)
Definition of osteoporosis
Decreased bone mass and micro architectural deterioration leading to increase in bone fragility and susceptibility to fracture
Bone mineral density >=2.5SD below the peak bone mass for young adults
( T-score <= -2.5)
Definition of osteopenia
Bone mineral density with T-score between -1 and -2.5
Cause of primary osteoporosis
Post-menopausal women have less oestrogen which results in resorption>mineralisation
Older men have less testosterone (to be converted to oestrogen)
Causes of secondary osteoporosis
Bone marrow disorders (MM, lymphoma, leukaemia)
Endocrine (Cushings, hyperparathyroid, hyperthyroid, diabetes)
Drugs (steroids, androgen deprivation therapy, aromatase inhibitors)
Rheum: RA, SLE, ankylosing spondylitis
Investigations for osteoporosis
DXA scan (bone scan) Lateral spine x ray looking for crush fractures
Bloods: FBE, ESR, UEC, Ca, Vitamin D, TFT
Management of osteoporosis
Ca supplements
Vitamin D
Bisphosphonates
Surgery in extreme cases
What is osteomalacia and what are common causes?
Definition: Vitamin D deficiency leading to soft bones
Causes: CKD or CLD (inability to convert vit D to active form) Dietary deficiency of vitamin D Decr UV exposure Malabsorption
Describing a fracture (6)
- Where
- Integrity of skin/soft tissue (simple/complex/open/closed)
- Angle (transverse/spiral/oblique/comminuted/semgmental)
- Pattern of fracture (non-displaced/non-displaced/distracted/angulated/impacted/rotated/shortened)
- Pathological fracture
- Complications (malunion/nonunion i.e. failed bone healing)
DDX red hot painful swollen joint
Septic arthritis
Septic bursitis
Gout/pseudogout
Haemarthrosis
Cellulitis
Underlying osteomyelitis
Define OA
Degenerative arthritis - gradual wear and tear of hyaline CARTILAGE resulting in joint pain, stiffness and functional limitation
Clin ft OA
Pain and crepitus, worst during use/at end of day and relieved by rest and panadol
Asymmetrical
Weight gain (pain limits exercise)
NO systemic SX or signs of inflammation (not hot/red)
Exam: Decr ROM, Heberden’s (DIP) and Bouchard’s (PIP) nodes
Common sites: hands (DIP, PIP, CMC), hip, knee, lumbar and cervical spine
Risk factors for OA vs RA
OA: Old age (OA) Obesity (joint loading and low level inflammation) Female Fam HX, genes Diabetes (ineffective repair, AGEs) Trauma, physical/manual occupation
RA:
Genetics
Smoking
X-ray changes OA
LOSS:
Loss of joint space
Osteophytes
Subchondral cysts
Subarticular sclerosis
Mx OA
Exercise
Weight loss if overweight
PT and OT (aids, splints, cane, brace)
Analgesia: paracetamol
+/- NSAIDs (topical or oral +PPI)
(+/- intraarticular steroid or hyaluronic acid injections)
Joint replacement (hips, knees) for severe disabling OA
Inx for suspected OA
Exclude other causes (inflammatory, soft tissue, periarticular)
Bloods: Rh factor, ANA
Xray
+/- MRI (spinal OA for ?nerve compression and r/o AVN)
Synovial fluid analysis if an acute flare up with effusion (r/o inflammation)
Back pain DDX
- MSK (includes OA)
- Fractures
- Infection (discitis, osteomyelitis, abscess)
RED FLAG conditions:
- Abdo referred pathology (AAA, renal colic etc)
- Malignancy - primary or spinal mets
- Rheum - ankylosing spondylitis
- Spinal cord compression (disc prolapse, osteophytes) causing neurological deficit or cauda equina syndrome or sciatica
Define RA
Autoimmune inflammatory disorder primarily attacking the joint ( INITIALLY INVOLVING SYNOVIAL membrane and progressing to erode the cartilage and underlying bone)
Leads to decr ROM and deformity, but may also affect the lungs, heart and RBCs
Clin ft RA
Symmetrical involvement of joints (MCP, PIP, IP, wrist, shoulder, knee, cervical spine)
Deformed joints
Hot, red, swollen, painful, Stiff joints
-Worse in the morning, after rest or prolonged inactivity
- Better with gentle movement
+/- low grade fever, lethargy, fatigue, anaemia
Extra articular manifestations of RA
Anaemia of chronic disease
Skin: Rh nodules
Lungs: fibrosis, granulomatous nodules, pleural effusions
Heart: Pericarditis, pericardial effusion, incr risk PVD, MI, Stroke
Eyes: Sjogrens
Deformities of RA
Ulnar deviation Boutonniere deformity (flexion PIP, extension DIP) Swan neck (extension PIP, flexion DIP) Z thumb (subluxation and fixed flexion of MCP, hyperextension of IP)
Claw, hammer and mallet toes
Investigations for suspected RA
Bloods: Rh factor, Anti-CCP
-FBE, ESR, CRP
X-ray may be normal at onset (U/S or MRI to detect early changes)
Mx RA
Lifestyle: exercise, diet, education
- PT and OT
- NSAIDs and paracetamol
- corticosteroids (oral or intra-articular)
-DMARDs (methotrexate + folate first line)
Surgery for structural joint damage
Monitor ESR, CRP, SX
Steroids - side effects
Weight gain Osteoporosis AVN Cataracts, glaucoma PUD Infection Easy bruising Acne HTN, HLDaemia Hypokalaemia, hyperglycaemia Mood swings
Therapeutic INR range
2-3
Aspects to cover in INR review
What is their current INR?
What dose of Warfarin are they taking?
Compliance
Check last few INRs and review the dose changes that were made, if any.
How often are they having INRs done
Review current Warfarin dose according to most recent INR
Tell patient when to come in for next INR
Reversal agent of Warfarin
Vitamin K
FNOF - how will the leg be oriented?
Externally oriented with shortening of leg
Aspects of hand injury exam
Assess:
-Blood supply (radial and ulnar pulses; colour; temp; cap refill)
- Nerves (radial, ulnar, median sensory and motor)
- Tendons (FDP passive and active; FDS-hold down other fingers)
- Bones/joints
Diagnostic criteria for DM
Symptoms of hyperglycaemia AND raised venous glucose detected once.
OR Raised venous glucose detected on 2 separate occasions
OR HBA1C > 6.5%
Diabetic if:
- fasting venous glucose >= 7mmol/L
- random >= 11.1mmol/L
Impaired tolerance if:
- fasting glucose 6.1-6.9
- random 7.8-11
No diabetes
- fasting <=6
- random <7.8
What medical conditions can cause DM?
Medical:
- Cushings
- Pheochromocytoma
- Hyperthyroid
- Pregnancy
Drugs
- Steroids
- Thiazide diuretics
- Anti-psychotics
Complications of diabetes
Micro: retinopathy, nephropathy (peripheral and autonomic), neuropathy
Macro: accelerated and more severe atherosclerosis, PVD, CVD (MI) and stroke
Management T1DM
- Education
- Insulin (pump)
- Exercise: low intensity aerobic
- Diet (low GI - small regular meals throughout day)
- Yearly follow up for presence of complications: Retinal exam, PVD, urinary A:C spot test
- Monitoring: BSLs and HBA1C
Management of T2D
1st line: lifestyle modification
- Diabetic education programme (diabetic educator, endocrinologist/GP)
- RF modification: smoking, alcohol, statin, BP control
- Diet: low GI, low calorie low carb diet, high protein (dietician)
- Exercise: low intensity aerobic (PT)
Medications +/- insulin
Follow-up and regular R/Vs for complications (opthalmologist, podiatrist, endocrinologist)
What does the HBA1C reflect and indicate?
reflects mean glucose level over previous 8 weeks
directly related to risk of complications
What is the first sign of nephropathy in a diabetic?
What test would you perform to detect this?
Management of nephropathy
First sign is microalbuminuria -> elevated Albumin: creatinine ratio (A:C spot urine test) but no protein so isn’t picked up on dipstick
MX: ACE inhibitor (‘pril) or ARB (Sartan)
What Diabetic medications can cause hypos and weight gain?
Sulfonylurea causes both
Glitazones (thiaz.) causes weight gain
What is first line medication for DM?
Mechanism?
SE?
CI?
Biguanides (Metformin)
Mechanism: incr insulin sensitivity and decr liver gluconeogenesis
SE: Nausea, diarrhoea
CI: renal failure (eGFR<36)
What happens if metformin isn’t controlling the BSLs adequately?
Then if still high after that, then what?
- ADD Sulfonylurea (unless BMI>35 then use gliptins which are weight losing)
3A. If still high, oral triple therapy: ADD Glitazone, glisten, acarbose
OR 3B. Oral + Insulin (basal or premix)
- Insulin: basal + pre-meal
What diabetic medications are weight losing?
Gliptins (decr gastric emptying to incr satiety)
SGLT2 inhibitors increase glucose excretion in renal tubules so you pee out glucose
What are the stages of diabetic eye disease and the changes that accompany each
Non-proliferative
- Micro aneurysms
- Blot haemmhorages
- Hard exudates (lipid deposits)
- cotton wool spots (infarcts)
- Venous beading
Proliferative retinopathy
- Neovascularisation due to local hypoxia and ischaemia (new vessels are abnormally frail and grow in wrong places)
- Large vitreal haemmhorages from new vessels -> VISION LOSS
- Glaucoma from neovasc.
Maculopathy
1. retinal detachment -> vision loss
Clinical features of diabetic peripheral neuropathy
® Injury or infection over pressure points
® Decr sensation in “glove and stocking” pattern
® Absent ankle jerks
® Neuropathic deformity (Charcot joint)
MX of hypoglycaemia
If conscious: oral fluids containing sugar or 6 jelly beans, then retest after 15min.
If >4, eat a longer acting CHO (sandwich). If <4 eat another 6 jelly beans.
If unconscious: IM/SC glucagon or IV 50% dextrose
Recheck BSL 20-30min later to see if further treatment required
What to ask about when inquiring about autonomic neuropathy?
Dizziness on standing (postural hypotension)
Sexual function
Faecal incontinence
Nausea after eating or full after eating a small amount (gastroparesis)
Definition and SX of hypoglycaemia
Definition - blood glucose <4mmol/L
- Autonomic symptoms from sympathetic overdrive
- sweaty, anxious, tremor, tachycardia, palpitations, dizziness
.2 Neuroglycopenic symptoms (similar to intoxication/psychosis)
- feeling irritable
- confusion, incoherence
- drowsiness
- visual trouble
- seizures
- coma
- sweaty
Triggers of DKA
Infection Inadequate insulin or new onset T1D Surgery MI Pancreatititis Chemo Drugs - Antipsychotics and Corticosteroids Psychosocial - etOH/other illicit substances, , eating disorders
SX of DKA
Polydipsia, polyuria
Abdo pain +/-nausea, vomiting
Lethargy, anorexia;
Altered conscious state/confusion, Drowsiness
Kussmaul hyperventilation (deep breathing)
Step by step approach to ECGs
- Identify the patient
- Rate
- Rhythm (SR, reg irreg, irreg irreg)
- PR (0.12-0.2s)
- QRS (<0.12s)
- QT (<1/2 RR interval) - Axis (I, II, aVF)
- Normal axis: all pos
- LAD: I pos, II pos/equi, aVF neg
- RAD: I neg, II pos, aVF pos - ST segment
What is 1st degree heart block
PR interval >0.2s (too long)
1 p wave per QRS but there is a delay
What is 2nd degree heart block
Occasional p waves not followed by QRS
Mobitz type 2: PR interval constant for conducted beats w occasional loss of QRS following p wave.
Weckebach: Progressive lengthening of PR interval followed by failure of conduction of atrial beat. Next PR interval is shorter than preceding.
what is third degree heart block
no relationship between p and QRS waves so PR interval is not constant
+/- narrow or wide QRS
Criteria for RBBB
rSR pattern in V1 (M)
W pattern in V6
Inverte T waves V2-V3
Criteria for LBBB
W pattern in V1
M pattern in V6
Inverted t waves V5-V6
ECG changes assoc w MI
Acute: ST elevation
Recent: T wave inversion
Old: Persistent Q waves (Q >33% of QRS height)
Causes acute liver disease
Paracetamol overdose
Acute viral hepatitis (A,B,E, CMV, EBV, YF)
Drugs
Autoimmune hepatitis
Causes of chronic liver disease
Chronic viral hepatitis (hep B, C, D) Autoimmune hepatitis Drugs Alcoholic liver disease NAFLD Haemochromatosis Wilson's disease
Long-term complications of HTN
Vasc - atherosclerosis and arteriolosclerosis, hyaline arteriolosclerosis, aortic dissection, berry aneurysm, aneurysms
Cardiac - IHD, MI, concentric LV hypertrophy, CCF
Kidneys - benign nephrosclerosis and hyaline arteriolosclerosis
Brain- shock, intracerebral haemmhorage, SA haemmhorage
Eye - hypertensive retinopathy
What do you have to monitor with statins?
LFT (hepatotoxicity)
CK (myopathy)
Management of hypercholesterolaemia
- Statins first line
- Add fibrate (lowers TGLs, incr HDL) or ezetimibe (lowers LDLs)
+/- fish oil
- 3 monthly bloods with est. diagnosis
Interpreting a snellen chart
As 6/number by line on chart that they
could read successfully (e.g. 6/5)
if the patient
read line 9 but got 1 letter wrong their acuity would be 6/9-1 (and vise-versa)
What nerve is affected in carpal tunnel?
SX
Inx
Mx
Median nerve as it passes under flexor retinaculum in the carpal tunnel
SX- numbness, pins and needles, night pain, weakness (opening jars, picking up coins, key in door), thenar wasting
Inx - ultrasound wrist, nerve conduction studies
Mx - wrist splints, C/S injections, surgical release, PT
Moves to test motor of:
- radial n.
- median n.
- ulnar n.
- Thumb abduction (point your thumb up to the ceiling and don’t let me push it down)
Wrist extension
Finger extension - Hold index and thumb together and don’t let me separate them (thumb and finger opposition)
- 5th finger abduction (don’t let me press it in)
Where to test sensory function of:
- Median n
- Ulnar n
- Radial n
- Median - index finger, radial aspect
- Ulnar - pinky
- Radial n - thenar eminence (palmar aspect)
SX of ACA stroke
Contralateral leg paresis and sensory loss
Sx of MCA stroke
Contralateral arm and face weakness and sensory loss
Eye deviation TOWARDS side of lesion
Dysphagia
L hem: aphasia
R hem: neglect
Sx of PCA stroke
Contralateral hemianopia or quadrantanopia
Visual changes
Amnesia, decreased consciousness
Lacunar infarcts
- how common are they?
- Where do they occur?
- SX
25% of all strokes
Basal ganglia, thalamus, internal capsule, pons
Typical stroke sydnromes ▪ Dysarthria clumsy hand ▪ Ataxia hemiparesis ▪ Pure motor hemiparesis ▪ Pure sensory
What are the 2 types of haemmhoragic stroke?
Causes of each
Intracerebral
• Usually in context of HTN
▪ Amyloid angiopathy
▪ Anticoagulants/drugs
▪ Vascular malformation
▪ Tumours can bleed
▪ Vasculitis can bleed
Subarachnoid
• Rupture of saccular/berry aneurysm or AVM
Secondary prevention for ischaemic stroke
Control RF • Smoking cessation ◦ BP <140 SBP <85 DBP (meds?) ◦ Lipids - statin ◦ ACEi ◦ Aspirin \+/- anticoagulant if in AF (CHADS2score) ◦ Carotid endartectomy or stenting if stenosis >70%
Cause-specific
• DC reversion of AF
• Stop hormone therapy
• PFO surgery
Physical activity/exercise
Limited exercise for control of diabetes, reduce alch, lose weight and promote a healthy diet
Secondary prevention for haemmhoragic stroke
BP control
Cause specific
• Eg: surgery for AVM
Avoid (will worsen bleeding)
• Antiplt
• Anticoag
• NSAIDs
Breast cancer screening program
Mammogram every 2 years for asymptomatic women
▪ NOTE: do NOT routinely examine the breasts of asymptomatic women - this is not in the guidelines
From age 50-75
High risk if fam HX <50yo or 2 first degree relatives -> get screening from 40yo
NOT for symptomatic women - these women need a breast exam, ultrasound and FNA
DDX breast lump
Breast cysts (fluid filled, can be painful) Fibroadenoma (smooth, firm, mobile, painless) Breast abscess (painful hot swelling) Duct ectasia (menopausal w nipple retraction and discharge) Fat necrosis (assoc w trauma/surgery)
Risk factors for breast cancer
Family HX Age Past history breast cancer Nulliparity 1st pregnancy >30yo Early menarche Late menopause HRT Obesity BRCA genes No breastfeeding
Markers for breast cancer and what they mean?
ER and PR (grow in response to oestrogen, and progesterone, respectively)
HER2 +++: aggressive disease
Triple negative disease is super aggressive , assoc w BRCA 1
Investigation of a suspicious breast lump
Triple assessment:
- Exam
- US/mammography
- FNA - core biopsy
SX of BPH
Voiding and storage SX
FUNWISE ▪ Frequency (S) ▪ Urgency (S) ▪ Nocturia (S) ▪ Weak stream (V) ▪ Intermittent stream (V) ▪ Straining (V) ▪ Emptying incomplete (V) = Hesitancy (V)
SX of prostate cancer
Asymptomatic commonly
Voiding and storage SX with locally advanced disease: FUNWISE
▪ Frequency (S)
▪ Urgency (S)
▪ Nocturia (S)
▪ Weak stream (V)
▪ Intermittent stream (V)
▪ Straining (V)
▪ Emptying incomplete (V)
+/- back/bone pain due to bony mets
MX BPH
- Watchful waiting and lifestyle (evening fluid restriction, planned voiding)
- Alpha-adrenergic antagonists (relaxes smooth muscle of prostate)
- 5Alpha reductase inhibitors (shrinks prostate)
- Anticholinergic (relaxes bladder muscle)
Surgery: TURP Laser ablation Open prostatectomy Stent
Complications of BPH and prostate cancer
Retention Overflow incontinence Hydronephrosis Infection Gross haematuria Bladder stones
Investigations for urinary obstruction in males
- DRE
- UEC and PSA
- Post-void residual or uroflow
OR Renal US ?hydronephrosis
OR Trans-urethral US guided needle biopsy
+/- CT/MRI (staging)
Investigations for LUTS in males
DRE
Urinalysis and culture (infx)
Bloods: UEC and PSA
Renal or abdominal US (?hydronephrosis, stones, urinary retention)
Trans-urethral US guided needle biopsy (BPH or prostate cancer req histological confirmation)
+/- CT/MRI (mets, staging)
Refer to urology if necessary
Management of COPD
COPD-X
Confirm Dx
- CXR, ECG, ABG, spirometry, DLCO
Optimise function
- Pulmonary rehab
- Medications: mild-mod Tiotropium (LAMA) and/or SABA prn; severe Salmeterol (LABA) +/- IC/S +/-LAMA +/- home O2
Prevent deterioration
- smoking cessation and vaccinate (flu and pneumococcus)
Develop self-management plan
X-acerbation management
- admit, low flow O2, C/S, bronchodilators, antibiotics, bipap/vpap, PT
Complications of COPD
Infective exacerbation
Hypoxia -> pulm HTN -> cor pulmonale
Chronic Bronchitis -> Small cell carcinoma
Emphysema -> pneumothorax
Indications for referral to urologist in elderly men w LUTS
Haematuria Recurrent infections Bladder stones Urinary retention Renal impairment
What tests should be done to investigate thyroid function?
- Blood TSH (if high, confirm T4)
Consider thyroid US if palpable goitre
Anti-TPO and Anti-TG antibodies (hashimoto)
Anti-TSH (Graves)
DO NOT need nuclear scan (unless they are thyrotoxic or have solitary nodule on U/S and want to know if it is hot or cold)
Treatment for hypothyroid
Thyroxine (needs to be taken separately from Iron, Ca, antacids which decr T4 absorption)
Adequate dietary Iodine
recheck TFTs after 6 weeks and adjust t4 dose if necessary
Causes of hyperthyroidism
- Graves
- Toxic nodular goitre (multinodular or solitary adenoma)
- Iodine induced (radiographic contrast, amiodarone)
- Factitious (too much T4 med)
- Transient (thyroiditis)
- Hypersecreting tumour within thyroid
What is a primary cause of hypothyroid?
What is the underlying pathophys and histology?
What blood tests would you do?
Goitre or no goitre?
“HASHIMOTO DISEASE”
- Autoimmune condition, T cell mediated (T4HS)
- Formation lymphoid follicles, germinal centres with mononuclear inflammatory infiltrate and hurthle cells
- Chronic inflammation, fibrosis/ scarring
- F>M
- Anti-Thyroglobulin and anti-TPO Abs
- T4 decrease and TSH increase
• Thyroid initially enlarges due to lymphocytic infiltration and fibsosis rather than hypertrophy, then atrophies over time
What are 2 primary causes of hyperthyroid?
- What is the pathophys?
- What would you see on bloods?
GRAVES DISEASE
- Autoimmune condition , B-cell (Ab) mediated (T2HS)
- F>M
- Production of thyroid-stimulating Igs (TSIs) from B cells stimulate TSH receptors on thyroid -> trophic effects on thyroid -> diffuse GOITRE and increased T3, T4
- Incr T3, T4 -> neg feedback -> lower TRH, TSH
HYPERSECRETING TOXIC MULTINODULAR GLANDS
• Nodules of hyper-plastic follicles become autonomous and start secreting T3 and T4
What signs are highly specific of graves disease?
Signs: oxopthalmus, pretibial myxoedema
congenital cause of hypothyroidism
mOther who is iodine deficient most commonly
What is cretinism?
hypothyroid from birth, causes dwarfism and severe mental retardation
Secondary cause of hyperthyroidism
Goitre or no goitre in this condition?
What would you see with TFTs?
Hypothalamic or anterior pituitary excess (tumour) drives TRH and TSH production -> TSH has trophic effect on thyroid -> GOITRE and increased T3, T4
-> neg feedback from incr T3, T4 unable to suppress excess TRH, TSH
Treatment for hyperthyroid
Surgery (risks damage to Recurrent laryngeal nerve and parathyroid)
FNA - assess for malignancy if suspected
Radioactive iodine^131 ablation (beta waves)
Drugs: carbemazole
Beta blockers treat SX from sympathetic overdrive
what would you see on bloods with subclinical hypothyroid?
What about subclinical hyperthyroid?
Do anything about it?
(compensated)
Hypo:
TSH high and T4 normal
No treatment
Hyper:
TSH low and T4 normal
YES because incr risk of AF and stroke! Treat w carbimazole
SX thyrotoxicosis
Nervousness, heat intolerance, palpitations, fatigue and weight loss (note: weight gain occurs in 10% of people)
Common examination findings include agitation, sinus tachycardia, fine tremor and hyper-reflexia, incr SBP and widened PP
SX hypothyroid
Puffy and pale facies Dry, brittle hair Sparse eyebrows Dry, cool skin Thickened and brittle nails Myxoedema – fluid infiltration of tissues
Cold intolerance
Weight gain
Fatigue
Reduced attention span Memory deficits Depression Headache Delayed reflexes
Bradycardia
Diastolic hypertension
Pericardial effusion
Decreased exercise tolerance
Anorexia
Constipation
Irregular or heavy menses
Infertility
5 alpha reductase - what does this enzyme do
converts testosterone to DHT
aromatase - what does this enzyme do? what does a deficiency in this enzyme mean?
Converts testosterone to estradiol
Deficiency in females means androgens circulate at high levels -> masculinisation
Clinical presentation of androgen deficiency: onset in adult men
General
- Decr sense of wellbeing, poor concentration, depression, irritability
- Fatigue, poor stamina
- Hot flushes, sweats
Sexual
- Reduced libido
- Decr erections
Signs
- Incr fat mass, decr muscle mass
- Gynaecomastia
- Osteoporosis
- Small/shrinking testes
Causes of erectile dysfunction
10% Psychological (if they get morning erection, wet dreams, can masturbate etc)
- sudden onset, sporadic and variable, still get morning erection, younger age, no organic RF
90% Organic:
Drugs
- anti HTN, anti depressants, anti-psychotics
Vascular (smoking, diabetes, HTN, CVD, pad, lipids)
Neurological - Nerves S2-4 (shoot) and PS (point) damage (surgery, spinal trauma, MS, PD, stroke)
Trauma - Penile damage
Hormonal
- Pituitary (ask about headaches and visual disturbance)
- thyroid
- hypogonadism
- cushing’s
Interpreting a snellen chart
As 6/number by line on chart that they
could read successfully (e.g. 6/5)
if the patient
read line 9 but got 1 letter wrong their acuity would be 6/9-1 (and vise-versa)
Treatment erectile dysfunction
Conservative ◦ Stop smoking, decr alcohol ◦ Sex counselling and education ◦ Change any precipitating meds ◦ Treat any underlying causes: DM, CVD, HTN, endocrinopathies
Oral medications (1st line) ◦ PDE5 inhibitors incr blood flow to penis temporarily: Sildenafil, Tadalafil, Vardenafil (valium)
Vaccuum devices (1st line) - draw blood into penis via neg pressure, then put ring at base of penis once erect
PGE1 analogue, Alprostadil (2nd line)
- Male urethral suppository for erection - pill inserted into urethra
- Self-injection
Surgical
◦ Penile implant
◦ Penile artery reconstruction
Psychological causes
◦ CBT
◦ Psychosexual counselling
Screening for bowel cancer
FOBT on at least 2 stool samples- immunochemical (not affected by diet or taking iron tablets so is more sensitive than the guaiac fobt)
▪ Every 2 years (but gvmt is a bit slack so ensure they are getting it done somehow)
▪ From 50-75yo
NOT a good test for those
• W family history <55yo
• W 2 first degree rel, or 1 first degree and 1 second degree on same side of fam diagnosed at any age
• Need a colonoscopy every 5 years, from 50yo or 10 years before youngest rel was diagnosed
Exantatide (GLP1 inhibitors)
- No hypos w monotherapy
- Weight losing
- Injection twice daily
- 0.5-1% reduction HBA1C
- But limited long term evidence
Acarbose
- 0.5-0.8% reduction
- Weight neytral
- No hypos w monotherapy
- Often poorly tolerance - bloating and flatulence
- 3x/day dosing
SGLT2 inhib
- Pee out the sugar
- Weight losing
- But increases the risk of UTIs and thrush
Motivational interviewing for diabetes
Find out what they know about insulin and their diabetes
Current desire to start insulin
Current ability to start insulin
Find out about their concerns
How committed/confident are they about starting insulin
• Rate 0-10
If they are scared about the pain and injections, you can show them a needle and practise giving an injection together (fake injection)
Explaining how to inject insulin
- Ensure you have discussed hypo sx and management BEFORE teaching them injection techniques
- Must be kept in the fridge but not in a place where they are likely to freeze
- Keep pens for up to a month before they must be thrown out
- ensure they are not overheated!
- Take foil cap off neede
- Put needle on pen
- Take clear and green caps off
- Dial up to 2units
- Press red bottom so insulin bead comes off top of needle
- Dial up # units insulin (10u is typical starting dose)
- Inject at 90 deg angle and parallel to floor
- Hold red button for 10 sec
- Recap needle
- Dispose of needle into sharps
Purpose of AUSDRisk assessment tool
What does high risk mean?
Screening of australians in primary care setting for risk of developing T2DM in the next 5 years
In Australia, patients with scores ≥12 (=HIGH RISK) in patients 40-49 should be investigated for possible diabetes (serum fasting blood glucose (FBG) or HbA1c) and enrolled for lifestyle intervention programs (advice regarding diet, weight control, and exercise) - will have ANNUAL blood test to monitor + continual monitoring of CVD RFs (weight, WC, BP, lipids)
Factors putting you at HIGH RISK of developing T2DM
- AUSDRISK score >= 12
- Any age with impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)*
- HX of CVD, stroke or PVD
- Age ≥35 years from the Pacific Islands, Indian subcontinent or China
- age ≥40 years + (BMI) ≥30 OR HTN
- Hx GDM
- PCOS
- Antipsychotic medication
Screening for diabetes in high risk population vs low risk population
Those considered at high risk should have an FBG or HbA1c test every three years.
Low risk: screening every 3 years from age 40 (or 18 if Ab/TSI) via AusDRisk calculator
High risk CVD risk assessment score
> =15
Provide frequent and sustained lifestyle advice, support and follow-up (CBR)
Commence BP + lipid lowering therapy
unless contraindicated or clinically inappropriate (EBR: Grade B)
Monitor individual risk factor response to treatment
Review new absolute risk of CVD
CVD risk assessment
Already at high risk and not requiring CVD risk assessment
• Diabetes and age >60 years
• Diabetes with microalbuminuria (> 20 mcg/min or urinary albumin:creatinine ratio >2.5 mg/mmol for males, >3.5 mg/ mmol for females)
• Moderate or severe chronic kidney disease (persistent proteinuria or estimated glomerular ltration raterate [eGFR] <45 mL/min//1.73 m2)
• A previous diagnosis of familial hypercholesterolaemia
• Systolic blood pressure ≥180 mmHg or diastolic blood pressure
≥110 mmHg
• Serum total cholesterol >7.5 mmol/L
People >45yo and not known to be high risk get risk assessment via cvdcheck.org.au
CVD risk assessment score - mod vs low risk management
Low risk - Brief, general lifestyle advice regarding diet and physical activity.
Appropriate advice, support and pharmacotherapy for smoking cessation
Mod risk
- diet and physical activity.
- Appropriate advice, support and pharmacotherapy for smoking cessation.
- Lifestyle advice given in preference to drug therapy.
- Consider BP lowering and/or lipid lowering in addition to lifestyle advice if 3-6 months of lifestyle intervention does not reduce risk or BP persistently >160/100 or fam HX premature onset CVD
Assoc ft to ask on HX about back pain
- HX trauma
- EVER been an IVDU (abscess)
- SX of fever, night sweats, LOW (abscess, malignancy)
- Bladder/bowel dysfunction (neurol/cauda equina)
- Saddle anaesthesia (cauda equina)
- Past HX cancer
- Are they getting severe or progressive neurological deficits (sciatica)
- Age of onset <20, >55 -> more worried
- Morning stiffness (rheum)
Indications for imaging in back pain
Indicated with
• Red flags
• Prologued neurological SX
No imaging
• Acute back pain, no red flags and improves within one month
• Chronic low back pain
Immediate imaging • X-ray and bloods • Major risk factors for cancer • MRI • Neurol deficits • Cauda equina • Abscess/spinal infection
Delayed imaging if • The patient returns with non-resolving back pain after around a month • XR+/-inflamm • Weak RF for cancer • Risk of ank spond • Risk of crush # • MRI • Radiculopathy (James) • Spinal stenosis
Yellow flags - define and give examples
• Psychosocial risk factors for persistence of pain
◦ Depression and social withdrawal
◦ Social or financial problems - Inability to return to work
◦ Negative attitude
◦ Fear/avoidance behaviour - spending time in bed
◦ Expectation for passive treatment (imaging, medications)
Risk assessment - depression
- Prev or current self harm
- Substance abuse
- Thoughts of suicide/life not worth living
- Intent
- Plans and arrangements made
- Past history of suicide attempts
- Fam hx suicide
- Protective factors - what’s stopping him from committing suicide
- Marital status (Divorced is higher risk)
- Feelings of guilt and hopelessness
- Recent stresses or losses
Management of depression in GP
Assess and manage risk ◦ Risk assessment ◦ Lifeline number ◦ ATAPS suicide prevention service ◦ Crisis assessment team referral ◦ Involuntary treatment under MHA Lifestyle ◦ Activity scheduling ◦ Sleep hygiene ◦ Relaxation exercises ◦ Exercise - mod intensity exercise ◦ Cut down on alcohol and caffeine Psychotherapy ◦ CBT • Face to face • Need mental health treatment plan to access 10 free sessions through medicare or can go private without care plan
Medications ◦ SSRIs - first line ◦ Others • SNRIs • Mirtazepine (NA specific antidepressant) • Agomelatin • Moclobemide - MAOi • TCAs ◦ ECT Frequent reviews
Mental health care plan requirements
Diagnosis of a mental health condition (not dementia, delirium, tobacco use disorder, mental retardation) HOPC Past history Crisis plan Outcome measure - K10
How do you assess bleeding risk?
HAS BLED score (each = 1)
Hypertension SBP >160 Abnormal renal (1) or liver function (1) Stroke previously Bleeding disorders Labile INR (<60% in therapeutic range) Elderly >65yo Drugs (aspirin or NSAIDs =1 + alcohol=1)
Score 2 - moderate risk of major bleeding event in 1 year
Score >2 - high risk, consider alternative to anticoagulation
CI to warfarin
- Pregnancy (teratogenic)
- Known large oesophageal varices
- Sig thrombocytopenia (platelets <50x109/L)
- Acute clinically significant bleed
- Within 72 hours of major surgery
- Decompensated liver disease or deranged baseline INR screen (>1.5)
Medication Counselling Framework
Assess prior understanding Explain Indication for tx Mechanism Dosing + duration: - how and when do they need to take it? - How to start it? - How long will they be on it for? Side effects and CI
Monitoring e.g. INR for Warfarin, Lithium levels – UEC, TFT, thyroxine – TSH
Special instructions e.g. dietary Vit K for Warfarin
Ask the patient if they have any questions
Histopathology of coeliac disease: 3 features
- Villous atrophy and crypt hyperplasia
- Increased #s plasma cells and lymphocytes in LP
- Increased IELs (CD4 T cells)
What sort of anaemia is associated w Coeliac disease?
Iron deficiency (microcytic)
or pernicious anaemia (B12, macrocytic)
What part of bowel does coeliac mainly affect? What affect does this have on absorption?
Duodenum and jejunum
Affects absorption of Vitamin B, C and folate (proximal), mostly
Protein, fat and fat soluble vitamins (A, E, D, K) distally. absorbed so only affected in severe disease.
Diagnosis of coeliac
Small bowel biopsy before starting GF diet
Bloods: FBE, Iron studies, UEC, B12, folate
Serology (anti gliadin and anti tTG antibodies + IgA)
HLA-DQ typing
Potential complications of UC vs Crohns
Crohns:
- Strictures
- Fissures -> risk of perforation
- Abscess
- Fistulae
- Perianal disease
US
- toxic megacolon -> risk of perforation
- incr risk colon cancer
What are the main symptoms for Crohn’s vs UC
Crohns: abdominal cramps, diarrhoea, weight loss (malnutrition), fever
UC: rectal bleeding, urgency, tenesmus, abdominal cramps
Extra colonic manifestations of Crohn’s vs UC
Crohns
- perianal fistulae and skin tags
- renal stones
- cholelithiasis
- oral ulcers
Both
- rashes, erythema nodosum
- arthritis, analysing spondylitis
- uveitis, episcleritis
- PSC
- fatty liver
Treatment of IBD
Crohns: stop smoking + only fluids during exacerbation
- Steroids (C-oral pred; UC-IV methylpred)
- 5ASA therapy +/- antibiotics
- Immunosuppressants (azathioprine, methotrexate, infliximab)
- Surgery for:
- Crohn’s: presence of complications
- UC: failed medical therapy, toxic megacolon, bleeding, pre-cancerous change
What is the criteria for IBS?
DIAGNOSIS OF EXCLUSION
Abdo pain relieved w defecation
Abdo pain assoc w change in fréquency OR consistency of stool
+/- bloating, passing mucus, straining, urgency, incr or decr stool frequency
Where does diverticular disease usually affect? where is the pain generally felt?
Sigmoid colon
LLQ
Management of diverticular disease
Diverticulosis: high fibre diet, avoid seeds and nuts.
Diverticulitis (acute episode):
- Conservative: NPO, IV fluids and IV cef and met
- surgical treatment is Hartmann procedure if refractory to medical MX, or complications present.
Causes of small vs large bowel obstruction
SMALL:
Functional (ileus)
Mechanical obstruction
- Adhesions
- Bulge (Hernias)
- Cancer (adenocarcinoma)
Rare causes
- foreign body
- intusseption
- Crohns stricture
- Gallstone ileus (stone lodges in ileocaecal valve - v rare!!)
LARGE:
Functional (ileus)
Mechanical obstruction
- Cancer
- Diverticulitis
- Volvulus
Rarer causes
- Adhesions
- Constipation
- Volvulus (sigmoid or caecal)
Gastritis - common causes of acute vs chronic
ACUTE Alcohol ASpirin/NSAIDs Stress H. Pylori
CHRONIC: H. Pylori Diet Environment Autoimmune NSAIDs Radiation Coealic (lymphocytic) Drugs (lymphocytic) Food allergies (eosinophilic) Crohn's , Sarcoidosis (non-infectious granulomatous)
Diagnosis of H pylori
Urea breath test
Serology and stool Ag test
Biopsy -> histology, rapid urease test
Management of Peptic Ulcer Disease
Depends on etiology!
◦ Stop NSAIDs if possible (replace w acetaminophen) ◦ Start PPI (inhibit H/K ATPase pump on parietal cells which secrete acid into lumen) ◦ Stop smoking ◦ Avoiding caffeine, alcohol, spices helps prevent SX ◦ Eradicate H. Pylori (Triple therapy for 7-14 days
- PPI
- Amoxicillin
- Clarithromycin)
What are the signs you get in the decompensation phase with CLD?
Encephalopathy -> drowsiness, metabolic flap
Jaundice
Ascitites + peripheral oedema
Leukonychia
Bruising/coagulopathy
Variceal bleeding
What is the coagulopathy in CLD due to?
How would you measure this - what blood test?
Lack of coagulation factors (factor VIII) due to impoaired synthetic function of liver
Low platelet count due to splenomegaly from portal HTN
-INR
Clinical features of acute viral hepatitis
Most subclinical.
Flu-like syndrome (nausea, vomiting, anorexia, headaches, fatigue, myalgia, fever, arthralgia)
Some progress to icteric phase - lasts days-weeks
- pale stool, dark urine, jaundice
- hepatomegaly, RUQ pain
- splenomegaly, cervical lymphadenopathy
treatment biliary colic vs acute cholecystitis
Bilairy colic: analgesia and rehydration with elective cholecystecomy
Acute cholecystitis:
- admit, hydrate, NPO, NG tube, analgesics
- cefazolin
- cholecystectomy early
where does most pancreatic cancer occur (what part of hte pancreas?) and how does it manifest clinically?
Head of the pancreas in 70%
- Systemic SX, obstructive jaundice, vague constant mid-epigastric pain, painless jaundice, courvoisier’s sign
+/- palpable tumour mass
DDX dysphagia
Trouble swallowing
- Structural
- Neurological
- Muscular
Stuck in throat:
a. Solids and liquids -> oesophageal motility disorder (achalasia, scleroderma, diffuse oesophageal spasm)
b. Solids only -> physical obstruction (carcinoma, peptic stricture, rings due to eosinophilic esophagitis, oesophageal diverticulum, oesophageal compression)
Indications for endoscopy with reflux
Failure of primary/empirical treatment Chronic GI bleeding Progressive unintentional weight loss Progressive difficulty in swallowing Persistent vomiting Iron deficiency anaemia Epigastric mass new onset in over 50
Complications with GORD
- Esophagus stricture disease (scarring can lead to dysphagia)
- Ulcer
- Bleeding
- Barrett’s esophagus and esophageal adenocarcinoma
Pathophys Barrett’s oesophagus
- Metaplasia of normal squamous esophageal epithelium to abnormal columnar epithelium containing intestinal metaplasia
- Cause: longstanding GORD causing damage to the oesophagus squamous epithelium -> esophagus wants to be more like the stomach which has a columnar epithelium
- Rate of malignant transformation is 0.12% per year
MX
- PPI
- endoscopy every 3 years if no dysplasia
- dysplasia -> endoscopic ablation/resection
1st vs 4th degree haemorrhoids
Relative tx
1st degree are completely internal - can bleed but aren’t painful and don’t prolapse (only seen on proctoscope)
tx - high fibre diet, avoid constipation and straining (stool softeners), haemmoroid creams (analgesic)
2nd-3rd tx: diet + rubber band ligation or injection sclerotherapy for bleeding
or surgery: haemorrhoidectomy
4th - prolapsed, non-reducible + thromboses and painful
tx- analgesia + surgery
Perianal bleeding (blood on toilet paper not mixed in)
Things to ask on bleeding
DDX
Pain Bleeding Lumps, swelling Itchiness Discharge
DDC
- haemmharoids (painless)
- anal fissure (painful)
- perianal abscess (red swollen tender lump + fever)
- anorectal fistula (mucus discharge, irritation, bleeding, 2dary to procedure)
- perianal haematoma (acutely painful perianal swelling, smooth purplish lump on exam)
- rectal prolapse (anal lump, bleeding, dischage, incontinence)
- anal warts
- pruritus ani (itch +/- bleeding)
- anal cancers (bleeding, lump, discharge, +/- pain; HPV related)
- low rectal cancer (bright red bleeding, mucus, tenesmus)
Mx anal fissure
1st line
◦ Topical GTN - complication is vascular headache
◦ OR diltiazem cream (Ca channel blocker)
◦ Movicol (laxative)
◦ ‘Haemmaroid cream’ - local anaesthetic just before they go to toilet.
2nd line
◦ Botox - lasts several months, is fully reversible and has 60-70% success rate
3rd line
◦ Lateral sphincterotomy (Post-surgical complication is incontinence)
- Severe nose bleeds and post-surgery bleeding (predominantly mucosal bleeding)
- Autosomal dominant inheritance
- Mildly elevated APTT
What is the provisional diagnosis and what test would confirm this??
Mild type 1 vWF deficiency
Confirm via blood tests for:
vWF Ag levels
vWF activity or function tests
- X-linked inheritance
- Characterised by joint bleeding! (often post-trauma)
- Mildly elevated APTT
What is the provisional diagnosis and what test would confirm this?
Mild Type Haemophilia
Confirm via blood tests for factors 8 (deficiency=Type A) and 9 (deficiency=Type B)
And/or genetic tests
- Bruising and petechiae on skin +/- Blood blisters on palate/mucosal surfaces, epistaxis, menorrhagia, GI bleeding, intracranial bleeding…
- Previously well with no medications
- Only abnormality on investigation is thrombocytopenia
What is the provisional diagnosis?
Treatment for this?
Immune Thrombocytopenia Purpura (ITP)
Diagnosis of exclusion!
Make sure to do FBE, blood film, U&Es, LFTs (can lead to renal failure), ANA, serology for EBV & CMV
Treatment:
- High dose steroids
- IV Ig if bleeding
- Splenectomy if life-threatening bleeding
- DO NOT give plts
- Arterial or venous blood clots
- Mixing study not correctable - what does this mean and what further bloods would you order for diagnosis?
What is the provisional diagnosis ?
indicating presence of an inhibitor rather than factor deficiency
-Blood tests positive for anticardiolipin and antiphospholipid Ab
Antiphospholipid syndrome (primary or secondary to SLE or induced by drugs such as Quinine)
- HX severe trauma, obstetric complications, sepsis, allergic/toxic reaction, cancer
- Investigations reveal: Low Hb and Plt; high APTT and PT; low fibrinogen; positive D dimer
What is the provisional diagnosis ? What is the underlying pathophys?
Disseminated Intravascular Coagulation
Widespread activation of clotting cascade results in formation of clots in microvasculature around body, leading to organ infarct and coagulation factor deficiency which leads to bleeding at other sites.
Differentials for abnormal bleeding
Haemophilia A or B vWF disorder Other factor deficiency Platelet disorder (ITP, TTP etc) Anticoag/antiplatelet drugs
DIC
CLD
Causes microcytic anaemia
Iron deficiency (slow chronic bleed or nutrient deficiency)
Anaemia of chronic disease
Thalassaemia
Causes normocytic anaemic
Hypoproliferative
- leukaemia
- aplastic anaemia
- pure red cell aplasia
Hyperproliferative
- haemmhorage/bleed
- haemolytic anaemia (sickle cell, thalassaemia, spherocytosis, G6DP deficiency, haemolytic uraemia, DIC, TTP)
Causes macrocytic anaemia
Megaloblastic
-B12/folate deficiency
Non-megaloblastic
- cirrhosis, liver failure
- alcoholism
- myelodysplastic syndrome
- congenital bone marrow failure syndrome
- myeloproliferative disorders
- myeloma
DDX for petechiae/purpura/ecchymosis
- Thrombocytopenia
- ITP
- Secondary to meds, leukaemia, SLE, APL syndrome, vWF deficiency - Vascular disorders
- Senile purpura, HTN, Henoch Schonlein purpura - Coagulation problem
- DIC or Scurvey - MENINGOCCOCEMIA
HSP triad
purpura
arthritis
abdo pain
Causes of B12 deficiency
Absorption of B12 requires gastric acid and IF
- Atrophic gastritis (autoimmune - autoantibodies targeting IF)
- Pancreatic failure
- Post-gastrectomy -lack IF
- Crohn’s or resection of ileum
- Coeliac
- Vegan diet
What causes folate deficiency anaemia?
Alcoholics
Malnourished patients
Pregnancy
What cells are affected by AML and CML?
erythrocytes, mast cells, thrombocytes (plt), basophils, neutrophils, eosinophils, macrophages and monocytes
What cells are affected by ALL and CLL?
ALL - B cells, T cells, NK cells
CLL- B cells mostly
What is myeloma?
Neoplastic disease of plasma cells (Ab producing mature B lymphocytes)
Neoplastic plasma cells produce PARAPROTEIN M (abnormal Abs consisting of light protein only) which accumulates in organs and causes damage (i.e. damages kidneys and gets into urine)
SX of myeloma
Due to
Calcium levels high due to activation of osteoclasts, causing bone resorption
Renal failure - proteinuria
Anaemia (tiredness and fatigue)
Bony pain due to lytic lesions
What is Lymphoma?
Malignant proliferations of mature lymphocytes that accumulate in lymph nodes (lymphadenopathy) and sometimes spread to the blood and other lymphoid organs (spleen, liver, bone marrow etc)
What is Leukaemia?
Acute - Neoplastic disease of IMMATURE cells (blasts) in bone marrow. affects myeloid or lymphoid progenitor cells
Chronic - neoplastic disease of MATURE white blood cells in the bone marrow.
Affects more mature cells
You have too many WCCs but they are dysfunctional so immune function is impaired.
What is the protein in the urine from MM called?
Bence Jones protein (paraprotein M)
Genetic causes of too much clotting
Antiphospholipid syndrome Antithrombin III def Protein C or S def Factor V leiden Prothrombin gene mutation
2 types of lymphoma and their classic features
- Non-hodgkin’s lymphoma
- Mostly diffuse large B cell lymphoma (more aggressive but higher cure rates)
- T cell forms @ 30% - Hodgkin’s lymphoma
- Reed sternberg cells (double nuclei)
- neoplastic prolif of B lymphocytes
- young adults and elderly
- 20-40% assoc w EBV
- rubbery painless non tender lymphadenopathy (cervical, axillary, inguinal); may spontaneously change size
- alcohol can induce lymph node pain
Fever, weight loss, night sweats, hepatosplenomegaly, exertion dyspnoea
Anaemia, bleeding/bruising, infx w bone marrow involvement due to pancytopenia
Blood and urine results for a patient w multiple myeloma
FBE - Normochromic normocytic anaemia with rouleux on blood film
ESR high
UEC - high creatinine
CMP - high Ca
Albumin - low or normal
Serum electrophoresis - low IgG and IgA; high serum free light chains (kappa and lambda) , paraprotein M
Urine electrophoresis and analysis - Paraprotein M and proteinuria
DX, IX and MX:
Vertigo when rolling over in bed onto R side, passing within a minute
DX: BPPV (otoliths from utricle become loose and lodge in posterior SC canal - vertigo related to body position)
IX: Dix-Hallpike manoeuvre -> head turned towards right, after a minute he has vertigo AND rotational nystagmus
MX: Epley manoeuvre
What is vestibular neuritis?
Abrupt onset of vertigo and off balance with no hearing loss or tinnitus. Associated nystagmus.
Vertigo improves before balance does.
Lasts DAYS-WEEKS
Possibly due to viral inflammation of vestibular ganglion.
Features of Meniere’s disease
periodic vertigo + hearing loss + tinnitis (you have to have all 3 to be diagnosed)
+ feeling of fullness in ears
EPISODIC - last hours, get it a few times a week, then again in 6 months
MX of Meziere’s disease
Acute episodes:
- Prochlorperazine (DAantag) or diazepam (vestibular suppressants)
Maintenance therapy
- life-style (minimise stresses and caffeine)
- diet: Low salt diet
- Medications: thiazide diuretic +/- beta histidine
DDX Vertigo and relative time frames
- BPPV: <1min duration
- Meniere’s disease: 30min-1 day duration
- Vestibular neuritis: days-weeks
- Acoustic neuroma (elderly patients, tinnitis more common presentation than vertigo)
DDX dizziness (light-headedness)
Medical
- Haem: anaemia
- Heart: dysrhythmia
- Endocrine: hypoglycaemia
- Drugs: antihypertensives
Neurological:
- MS
- Migraine
features of COPD
insidious onset, morning productive cough, +/- wheeze, hx of smoking, tachypnoea, dyspnoea, pursed lip breathing, cyanosis, barrel chest, dear chest expansion, decr breath sounds, reasonant/hyperresonant
migraine mx
Prophylaxis:
propanolol
amitryptinine
Acute - NSAID +/- triptan
DDX fatigue
Depression, anxiety, stress/lifestyle OSA Thyroid DM post-viral infx Anaemia Malignancy Chronic disease: CCF, CLD, CRF
Testing hearing
Whisper test
Weber’s test - tuning fork in middle of forehead
- hearing ringing in midline is normal
- louder on L -> conductive hearing loss on L or sensorineural on R
Rinner’s - turning fork on maSTOID process until the ringing stops then move next to ear and ask if patient can still hear it
- can hear ringing = normal (AC>BC) = positive Rinne’s test
- cannot hear it = abnormal BC >AC = negative Rinne’s
- Conductive hearing loss if weber’s and Rinne’s on SAME side
- SN hearing loss if Weber’s and Rinne’s on OPPOSITE side
Acoustic neuroma features
What CN are affected
One sided hearing loss Vertigo Tinnitis Nausea Unilateral FACIAL WEAKNESS, tingling
(CN 5,7,8 affected)
Who is eligible for the Zostavax?
What does it do
70-79 year olds for the prevention of shingles (herpes zoster) and post-herpetic neuralgia
What do you have to be wary of with shingles involving the face?
MX of this
Herpes zoster opthalmicus, if lesions are on eye/nose
Affects ophthalmic branch of trigeminal nerve
Ophthalmological emergency because can threaten sight
MX - refer immediately + initiate antiviral therapy + topical steroid drops
Mx of post herpetic neuralgia
Commence tx early!!!
pain can last >1-4 months from initial onset of rash +/- other sensory sx
mx - neuropathic pain medications (pregabalin, gabapentin, amitryptiline)
Side effects of beta blockers
Bradycardia and hypotension orthostatic hypotensive Transient worsening of HF Bronchospasm (Care w asthma) Cold extremities - Exacerbate Reynolds Dizziness
Relative CI to betablockers
Cardiac
- bradycardia (45-50)
- heart block
- severe hypotension
- decompensated/uncontolled HF
Severe PAD (vasoconstrictor)
DM - can mask hypoglycaemia
Asthma (those metoprolol which is beta1 specific)
