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GP Flashcards

1
Q

What are some of the causes of secondary hypertension?

A

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)

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2
Q

How is the treatment protocol (pharm vs lifestyle modification) for different categories for HTN divided up?

A

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

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3
Q

Pharm. treatment (order of use) for HTN

A

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

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4
Q

What drug combinations to avoid in HTN and why? (3)

A
  1. Ace inhibitor + K-sparing diuretic (spironolactone) - risk of hyperkalaemia
  2. Ca channel blocker + beta blocker - risk of heart block
  3. ACEi + AT1R antag - not shown to be clinically effective
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5
Q

LONG-TERM Treatment protocol for CHF

A
  1. Lifestyle modification
    Smoking and alcohol cessation
    Na and fluid restriction
    Diet and exercise (weight control)
  2. Treat underlying cause and aggravating factors (valvular disease/arrhythmia; thyroid, infection, anaemia, HTN)
  3. 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

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6
Q

Precipitants/exacerbaters of heart failure

A 
MADHATTER:
MI/ischaemia
Anaemia
Drugs (NSAIDs, steroids, non-compliance)
HTN
Arrhythmias 
Thyroid
Toxic (infection)
Endocarditis/embolus
Renal failure
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7
Q

Stable angina vs unstable angina

A

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)
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8
Q

STEMI vs non-STEMI

A

STEMI: Criteria for MI + ST elevation or new BBB

NON-STEMI: Criteria for MI WITHOUT ST elevation or new BBB

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9
Q

Criteria for MI

A

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)
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10
Q

Long-term management of IHD post-acute ACS event (8)

A
  1. Dual anti-platelets (aspirin + clopidogrel)
  2. Beta blockers (Ca channel blocker second line)
  3. ACE inhibitors (prevent remodelling)
  4. Nitrates (GTN) PRN for symptom relief
  5. Statin (irrespective of cholesterol levels for plaque stabilisation)
  6. Modify lifestyle (exercise, diet, cease smoking, weight control, alcohol, stress)
  7. Modify CV Risk Factors (diabetes, cholesterol, HTN)
  8. Review (1 month then 6 mo thereafter)
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11
Q

Standard Management of dyslipidaemia

A

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.
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12
Q

What is the screening protocol for hyperlipidameia?

A

Full fasting lipid profile every 3 years for
○ Males > 40
○ Females > 50 (or menopausal)
○ Anyone with other CAD risk factors

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13
Q

Risk factors for AF

A

CHADS2

CCF
HTN
Age >75
DM
Stroke/TIA/Thromboembolus previously
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14
Q

Management of CHRONIC AF

A
  1. Evaluate stroke risk and manage -> score 0 gets aspirin; score >1 gets anticoagulation (warfarin or NOAC)
  2. Rate control if patient stable (beta blocker, diltiazem, verapamil or digoxin, or amiodarone last line)

Rhythm control (SOTOLOL. flecainide&raquo_space;> amiodarone if in HF) if patient is symptomatic or younger or has CCF

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15
Q

Triggers of AF

A 
Heart failure/ischaemia 
HTN
MI 
PE
Valvular disease (mitral)
Hyperthyroid
Caffeine/alcohol
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16
Q

Management of Acute AF (<48 hours)

A

If very ill or haemodynamically unstable:

  1. O2
  2. Emergency cardioversion (electrical or IV amiodarone if unavailable. Flecanide)
  3. Rate control (Verapamil or Bisoprolol = Ca channel or beta blocker; digoxin or amiodarone 2nd line)
  4. Anticoagulation (LMWH)

Treat any triggering illnesses (pneumonia, MI, PE etc)

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17
Q

Sx and signs of PAD?

A

SX:
Claudication
Rest pain

Signs:
Rubor 
Ulcers, gangrene, cellulitis
Abnormal nails
Shiny, hairless, cool/pale
Decr pulses
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18
Q

Management of intermittent claudication

A

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

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19
Q

Clinical presentation of chronic venous disease

A

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

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20
Q

What is venous disease caused by?

A

Venous HTN and venous insufficiency

causes of venous HTN (=OLD AGE)

  1. inadequate muscle pump function
  2. incompetent venous valves -> reflux
  3. venous thrombus or obstruction

Venous HTN leads to vein dilatation, skin changes and or ulceration

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21
Q

Treatment of peripheral venous disease

A

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)

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22
Q

Treatment varicose veins

A 
Compression stockings
Leg elevation
Injection sclerotherapy
Surgery - vein removal (Stripping, ligation)
Vein ablation
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23
Q

Characteristics of venous ulcers

A

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

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24
Q

Characteristics of arterial ulcers

A

VERY PAINFUL

Often on foot pressure point areas

Small size
Deep with punched out appearance
Regular margins
Sloughy/necrotic base

Absent pedal pulses

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25
Q

Neuropathic ulcer characteristics

A

Often very large but size and shape varies
NOT PAINFUL

Appearance: Prominent hypertrophied squamous rind around edge

Often on feet -pressure point areas

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26
Q

ECG anomalies assoc w syncope

A

Sinus bradycardia
Conduction block
Wolff Parkinson white syndrome

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27
Q

How to intensify the MR and AS murmurs

A

MR: get patients to roll onto L side and inspire

AS: Patient leans forwards and expires

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28
Q

Signs of RHF vs LFH

A

RHF: incr JVP, hepatosplenomegaly, ascites, peripheral oedema

LHF: pulmonary oedema -> lung crackles (SX: SOB, orthopnoea, PND)

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29
Q

Complications of HTN

A

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).
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30
Q

Treatment rosacea

A

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!

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31
Q

Characteristics of rosacea

How is this different from acne?

A

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

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32
Q

Contact dermatitis - compare the 2 types

A

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.
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33
Q

Eczema vs Psoriasis

Signs

A

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

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34
Q

Eczema treatment

chronic vs acute flare

A

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)

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35
Q

1-2 weeks after strep URTI.

Guttate psoriasis. (small plaque psoriasis, almost looks like red mosquito bites)

A

Which type of psoriasis is associated w strep pharyngitis (strep throught)?

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36
Q

BCC characteristics

A

Pearly/transulent firm nodule
Rolled edges
+/- central indentation or ulceration (“rodent ulcers”)

Telangiectic border (red)
painless bleeding

Indolent growth

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37
Q

SCC characteristics

A

Erythematous nodule or plaque
Hyperkeratotitic surface crust (keratinocyte proliferation)
Ulceration, bleeding

Grows quickly, over weeks-months
May be tender to palpation

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38
Q

SCC

  1. level of invasion
  2. where are they found?
A
  1. More likely to spread than BCC (to regional lymph nodes first)
  2. Sun exposed sites
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39
Q

Management of SCC

A

COMPLETE wide local excision with biopsy +/- adj. radiotherapy

Not for surgery: radiotherapy alone

lifelong follow up

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40
Q

Descibring skin lesions ABCDE

A 
Asymmetry
Borders (irregular)
Colour (variated)
Diameter (>6mm)
Evolution
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41
Q

WHAT WOULD you use to characterise the prognosis of melanoma?

A

Breslow thickness - thickness of lesion based on biopsy histology determines recommended margin for wide local excision

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42
Q

What do you do about a suspicious lesion if they are:

  • Raised
  • Flat
  • Pigmented/suspicious for melanoma
A

Raised: shave biopsy

Flat:

  • Large: Punch biopsies of most suspicious areas
  • Small: Wide excision if small

Pigmented/melanoma - complete wide excision

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43
Q

DX, investigations and treatment: itchy rash with a gradually enlarging red scaly edge and clearing central pale region

A

Tinea Corporis (ring worm)

  • Fungal infection -> skin scraping for fungal MCS
  • Treat with topical anti fungal cream (imidazole)
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44
Q

What is the significance of solar or actinic keratosis ?

What are red flags?

What do you do about them?

A

10% can develop to SCC

Watchful waiting

If suspicious for transformation to SCC (growing, hyperkeratotic, TENDER):

Cryotherapy
Topical medications (5-Fu, imiquimod)
Surgical excision

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45
Q

Actinic keratosis:

Where are they generally found and what are key features?

A

Found on sun exposed skin - face, scalp, forearms and hands

Scaly erythematous lesions, sand-papery texture +/- actinic horn

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46
Q

What is Bowen’s disease?

Appearance?

SX?

What is the significance of them?

A 
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.

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47
Q

Topical meds for removing skin lesions

A

5-fluorouracil cream
Imiquimod cream (IFN)
Photodynamic therapy

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48
Q

BCC

  1. level of invasion
  2. where are they found?
A

Local invasion (almost never metastasise)

Found on face

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49
Q

What causes warts?

Treatment of warts

A 
HPV infection
Destructive
- liquid nitrogen
- diathermy
- curettage

Topical

  • salicylic acid (keratolytics)
  • DCP immunotherapy
  • Imiquimod (genital warts)
  • Tape
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50
Q

Impetigo: what is the generic name?

What organism causes impetigo and what is the characteristic appearance?

A

“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.

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51
Q

Treatment for psoriasis

A

Topical therapy
-steroids, topical vitD, keratinolytics
Emollients

UVB phototherapy

Systemic immunosuppressants and biologic agents

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52
Q

Sites where psoriasis is usually found

A

Extensor surfaces
Scalp
AnoGenital (more of a glazed appearance, less scaly)
palmar and plantar surfaces
Nails - psoriatic arthritis more likely with nail involvement

Auricular

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53
Q

Cellulitis: common causative agents

TX

A

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

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54
Q

Management acne

A

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.
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55
Q

Features of acne

A

Comedones (open are black heads and closed are white heads)
Papules (no pus), pustules (pus)
Nodular pseudocysts
Scarring

Hormonal - Onset in adolescence
Genetic

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56
Q

complications of rosacea

A

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)

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57
Q

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.

A

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)

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58
Q

What virus causes shingles?

A

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

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59
Q

DX, investigations and treatment: itchy rash with a gradually enlarging red scaly edge and clearing central pale region

A

Tinea Corporis (ring worm)

  • Fungal infection -> skin scraping for fungal MCS
  • Treat with topical anti fungal cream (imidazole)
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60
Q

Definition of osteoporosis

A

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)

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61
Q

Definition of osteopenia

A

Bone mineral density with T-score between -1 and -2.5

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62
Q

Cause of primary osteoporosis

A

Post-menopausal women have less oestrogen which results in resorption>mineralisation

Older men have less testosterone (to be converted to oestrogen)

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63
Q

Causes of secondary osteoporosis

A

Bone marrow disorders (MM, lymphoma, leukaemia)

Endocrine (Cushings, hyperparathyroid, hyperthyroid, diabetes)

Drugs (steroids, androgen deprivation therapy, aromatase inhibitors)

Rheum: RA, SLE, ankylosing spondylitis

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64
Q

Investigations for osteoporosis

A 
DXA scan (bone scan)
Lateral spine x ray looking for crush fractures

Bloods: FBE, ESR, UEC, Ca, Vitamin D, TFT

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65
Q

Management of osteoporosis

A

Ca supplements
Vitamin D
Bisphosphonates

Surgery in extreme cases

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66
Q

What is osteomalacia and what are common causes?

A

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
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67
Q

Describing a fracture (6)

A
  1. Where
  2. Integrity of skin/soft tissue (simple/complex/open/closed)
  3. Angle (transverse/spiral/oblique/comminuted/semgmental)
  4. Pattern of fracture (non-displaced/non-displaced/distracted/angulated/impacted/rotated/shortened)
  5. Pathological fracture
  6. Complications (malunion/nonunion i.e. failed bone healing)
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68
Q

DDX red hot painful swollen joint

A

Septic arthritis
Septic bursitis
Gout/pseudogout
Haemarthrosis

Cellulitis
Underlying osteomyelitis

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69
Q

Define OA

A

Degenerative arthritis - gradual wear and tear of hyaline CARTILAGE resulting in joint pain, stiffness and functional limitation

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70
Q

Clin ft OA

A

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

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71
Q

Risk factors for OA vs RA

A 
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

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72
Q

X-ray changes OA

A

LOSS:

Loss of joint space
Osteophytes
Subchondral cysts
Subarticular sclerosis

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73
Q

Mx OA

A

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

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74
Q

Inx for suspected OA

A

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)

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75
Q

Back pain DDX

A
  1. MSK (includes OA)
  2. Fractures
  3. Infection (discitis, osteomyelitis, abscess)

RED FLAG conditions:

  1. Abdo referred pathology (AAA, renal colic etc)
  2. Malignancy - primary or spinal mets
  3. Rheum - ankylosing spondylitis
  4. Spinal cord compression (disc prolapse, osteophytes) causing neurological deficit or cauda equina syndrome or sciatica
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76
Q

Define RA

A

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

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77
Q

Clin ft RA

A

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

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78
Q

Extra articular manifestations of RA

A

Anaemia of chronic disease

Skin: Rh nodules

Lungs: fibrosis, granulomatous nodules, pleural effusions

Heart: Pericarditis, pericardial effusion, incr risk PVD, MI, Stroke

Eyes: Sjogrens

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79
Q

Deformities of RA

A 
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

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80
Q

Investigations for suspected RA

A

Bloods: Rh factor, Anti-CCP
-FBE, ESR, CRP

X-ray may be normal at onset (U/S or MRI to detect early changes)

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81
Q

Mx RA

A

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

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82
Q

Steroids - side effects

A 
Weight gain
Osteoporosis
AVN
Cataracts, glaucoma
PUD
Infection 
Easy bruising
Acne
HTN, HLDaemia
Hypokalaemia, hyperglycaemia
Mood swings
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83
Q

Therapeutic INR range

A

2-3

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84
Q

Aspects to cover in INR review

A

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

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85
Q

Reversal agent of Warfarin

A

Vitamin K

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86
Q

FNOF - how will the leg be oriented?

A

Externally oriented with shortening of leg

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87
Q

Aspects of hand injury exam

A

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
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88
Q

Diagnostic criteria for DM

A

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
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89
Q

What medical conditions can cause DM?

A

Medical:

  • Cushings
  • Pheochromocytoma
  • Hyperthyroid
  • Pregnancy

Drugs

  • Steroids
  • Thiazide diuretics
  • Anti-psychotics
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90
Q

Complications of diabetes

A

Micro: retinopathy, nephropathy (peripheral and autonomic), neuropathy

Macro: accelerated and more severe atherosclerosis, PVD, CVD (MI) and stroke

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91
Q

Management T1DM

A
  • 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
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92
Q

Management of T2D

A

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)

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93
Q

What does the HBA1C reflect and indicate?

A

reflects mean glucose level over previous 8 weeks

directly related to risk of complications

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94
Q

What is the first sign of nephropathy in a diabetic?
What test would you perform to detect this?

Management of nephropathy

A

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)

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95
Q

What Diabetic medications can cause hypos and weight gain?

A

Sulfonylurea causes both

Glitazones (thiaz.) causes weight gain

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96
Q

What is first line medication for DM?

Mechanism?

SE?

CI?

A

Biguanides (Metformin)

Mechanism: incr insulin sensitivity and decr liver gluconeogenesis

SE: Nausea, diarrhoea

CI: renal failure (eGFR<36)

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97
Q

What happens if metformin isn’t controlling the BSLs adequately?

Then if still high after that, then what?

A
  1. 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)

  1. Insulin: basal + pre-meal
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98
Q

What diabetic medications are weight losing?

A

Gliptins (decr gastric emptying to incr satiety)

SGLT2 inhibitors increase glucose excretion in renal tubules so you pee out glucose

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99
Q

What are the stages of diabetic eye disease and the changes that accompany each

A

Non-proliferative

  1. Micro aneurysms
  2. Blot haemmhorages
  3. Hard exudates (lipid deposits)
  4. cotton wool spots (infarcts)
  5. Venous beading

Proliferative retinopathy

  1. Neovascularisation due to local hypoxia and ischaemia (new vessels are abnormally frail and grow in wrong places)
  2. Large vitreal haemmhorages from new vessels -> VISION LOSS
  3. Glaucoma from neovasc.

Maculopathy
1. retinal detachment -> vision loss

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100
Q

Clinical features of diabetic peripheral neuropathy

A

® Injury or infection over pressure points
® Decr sensation in “glove and stocking” pattern
® Absent ankle jerks
® Neuropathic deformity (Charcot joint)

101
Q

MX of hypoglycaemia

A

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

102
Q

What to ask about when inquiring about autonomic neuropathy?

A

Dizziness on standing (postural hypotension)

Sexual function

Faecal incontinence

Nausea after eating or full after eating a small amount (gastroparesis)

103
Q

Definition and SX of hypoglycaemia

A

Definition - blood glucose <4mmol/L

  1. 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
104
Q

Triggers of DKA

A 
Infection
Inadequate insulin or new onset T1D
Surgery
MI
Pancreatititis
Chemo
Drugs - Antipsychotics and Corticosteroids
Psychosocial - etOH/other illicit substances, , eating disorders
105
Q

SX of DKA

A

Polydipsia, polyuria
Abdo pain +/-nausea, vomiting
Lethargy, anorexia;
Altered conscious state/confusion, Drowsiness

Kussmaul hyperventilation (deep breathing)

106
Q

Step by step approach to ECGs

A
  1. Identify the patient
  2. Rate
  3. Rhythm (SR, reg irreg, irreg irreg)
    - PR (0.12-0.2s)
    - QRS (<0.12s)
    - QT (<1/2 RR interval)
  4. Axis (I, II, aVF)
    - Normal axis: all pos
    - LAD: I pos, II pos/equi, aVF neg
    - RAD: I neg, II pos, aVF pos
  5. ST segment
107
Q

What is 1st degree heart block

A

PR interval >0.2s (too long)

1 p wave per QRS but there is a delay

108
Q

What is 2nd degree heart block

A

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.

109
Q

what is third degree heart block

A

no relationship between p and QRS waves so PR interval is not constant
+/- narrow or wide QRS

110
Q

Criteria for RBBB

A

rSR pattern in V1 (M)
W pattern in V6
Inverte T waves V2-V3

111
Q

Criteria for LBBB

A

W pattern in V1
M pattern in V6
Inverted t waves V5-V6

112
Q

ECG changes assoc w MI

A

Acute: ST elevation
Recent: T wave inversion
Old: Persistent Q waves (Q >33% of QRS height)

113
Q

Causes acute liver disease

A

Paracetamol overdose
Acute viral hepatitis (A,B,E, CMV, EBV, YF)
Drugs
Autoimmune hepatitis

114
Q

Causes of chronic liver disease

A 
Chronic viral hepatitis (hep B, C, D)
Autoimmune hepatitis
Drugs
Alcoholic liver disease 
NAFLD
Haemochromatosis 
Wilson's disease
115
Q

Long-term complications of HTN

A

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

116
Q

What do you have to monitor with statins?

A

LFT (hepatotoxicity)

CK (myopathy)

117
Q

Management of hypercholesterolaemia

A
  1. Statins first line
  2. Add fibrate (lowers TGLs, incr HDL) or ezetimibe (lowers LDLs)

+/- fish oil

  1. 3 monthly bloods with est. diagnosis
118
Q

Interpreting a snellen chart

A

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)

119
Q

What nerve is affected in carpal tunnel?

SX
Inx
Mx

A

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

120
Q

Moves to test motor of:

  1. radial n.
  2. median n.
  3. ulnar n.
A
  1. Thumb abduction (point your thumb up to the ceiling and don’t let me push it down)
    Wrist extension
    Finger extension
  2. Hold index and thumb together and don’t let me separate them (thumb and finger opposition)
  3. 5th finger abduction (don’t let me press it in)
121
Q

Where to test sensory function of:

  1. Median n
  2. Ulnar n
  3. Radial n
A
  1. Median - index finger, radial aspect
  2. Ulnar - pinky
  3. Radial n - thenar eminence (palmar aspect)
122
Q

SX of ACA stroke

A

Contralateral leg paresis and sensory loss

123
Q

Sx of MCA stroke

A

Contralateral arm and face weakness and sensory loss
Eye deviation TOWARDS side of lesion
Dysphagia

L hem: aphasia
R hem: neglect

124
Q

Sx of PCA stroke

A

Contralateral hemianopia or quadrantanopia
Visual changes
Amnesia, decreased consciousness

125
Q

Lacunar infarcts

  • how common are they?
  • Where do they occur?
  • SX
A

25% of all strokes
Basal ganglia, thalamus, internal capsule, pons

Typical stroke sydnromes
	▪	Dysarthria clumsy hand
	▪	Ataxia hemiparesis
	▪	Pure motor hemiparesis
	▪	Pure sensory
126
Q

What are the 2 types of haemmhoragic stroke?

Causes of each

A 
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

127
Q

Secondary prevention for ischaemic stroke

A 
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

128
Q

Secondary prevention for haemmhoragic stroke

A

BP control

Cause specific
• Eg: surgery for AVM

Avoid (will worsen bleeding)
• Antiplt
• Anticoag
• NSAIDs

129
Q

Breast cancer screening program

A

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

130
Q

DDX breast lump

A 
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)
131
Q

Risk factors for breast cancer

A 
Family HX
Age
Past history breast cancer 
Nulliparity
1st pregnancy >30yo
Early menarche
Late menopause
HRT
Obesity
BRCA genes
No breastfeeding
132
Q

Markers for breast cancer and what they mean?

A

ER and PR (grow in response to oestrogen, and progesterone, respectively)

HER2 +++: aggressive disease

Triple negative disease is super aggressive , assoc w BRCA 1

133
Q

Investigation of a suspicious breast lump

A

Triple assessment:

  • Exam
  • US/mammography
  • FNA - core biopsy
134
Q

SX of BPH

A

Voiding and storage SX

FUNWISE
	▪	Frequency (S)
	▪	Urgency (S)
	▪	Nocturia (S)
	▪	Weak stream (V)
	▪	Intermittent stream (V)
	▪	Straining (V)
	▪	Emptying incomplete (V)
= Hesitancy (V)
135
Q

SX of prostate cancer

A

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

136
Q

MX BPH

A
  • 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
137
Q

Complications of BPH and prostate cancer

A 
Retention
Overflow incontinence
Hydronephrosis
Infection
Gross haematuria
Bladder stones
138
Q

Investigations for urinary obstruction in males

A
  1. DRE
  2. UEC and PSA
  3. Post-void residual or uroflow
    OR Renal US ?hydronephrosis
    OR Trans-urethral US guided needle biopsy
    +/- CT/MRI (staging)
139
Q

Investigations for LUTS in males

A

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

140
Q

Management of COPD

A

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

141
Q

Complications of COPD

A

Infective exacerbation
Hypoxia -> pulm HTN -> cor pulmonale
Chronic Bronchitis -> Small cell carcinoma
Emphysema -> pneumothorax

142
Q

Indications for referral to urologist in elderly men w LUTS

A 
Haematuria
Recurrent infections
Bladder stones
Urinary retention 
Renal impairment
143
Q

What tests should be done to investigate thyroid function?

A
  1. 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)

144
Q

Treatment for hypothyroid

A

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

145
Q

Causes of hyperthyroidism

A
  • Graves
  • Toxic nodular goitre (multinodular or solitary adenoma)
  • Iodine induced (radiographic contrast, amiodarone)
  • Factitious (too much T4 med)
  • Transient (thyroiditis)
  • Hypersecreting tumour within thyroid
146
Q

What is a primary cause of hypothyroid?

What is the underlying pathophys and histology?

What blood tests would you do?

Goitre or no goitre?

A

“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

147
Q

What are 2 primary causes of hyperthyroid?

  • What is the pathophys?
  • What would you see on bloods?
A

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

148
Q

What signs are highly specific of graves disease?

A

Signs: oxopthalmus, pretibial myxoedema

149
Q

congenital cause of hypothyroidism

A

mOther who is iodine deficient most commonly

150
Q

What is cretinism?

A

hypothyroid from birth, causes dwarfism and severe mental retardation

151
Q

Secondary cause of hyperthyroidism

Goitre or no goitre in this condition?

What would you see with TFTs?

A

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

152
Q

Treatment for hyperthyroid

A

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

153
Q

what would you see on bloods with subclinical hypothyroid?

What about subclinical hyperthyroid?

Do anything about it?

A

(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

154
Q

SX thyrotoxicosis

A

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

155
Q

SX hypothyroid

A 
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

156
Q

5 alpha reductase - what does this enzyme do

A

converts testosterone to DHT

157
Q

aromatase - what does this enzyme do? what does a deficiency in this enzyme mean?

A

Converts testosterone to estradiol

Deficiency in females means androgens circulate at high levels -> masculinisation

158
Q

Clinical presentation of androgen deficiency: onset in adult men

A

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
159
Q

Causes of erectile dysfunction

A

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
160
Q

Interpreting a snellen chart

A

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)

161
Q

Treatment erectile dysfunction

A 
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

162
Q

Screening for bowel cancer

A

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

163
Q

Exantatide (GLP1 inhibitors)

A
  • No hypos w monotherapy
    • Weight losing
    • Injection twice daily
    • 0.5-1% reduction HBA1C
    • But limited long term evidence
164
Q

Acarbose

A
  • 0.5-0.8% reduction
    • Weight neytral
    • No hypos w monotherapy
    • Often poorly tolerance - bloating and flatulence
    • 3x/day dosing
165
Q

SGLT2 inhib

A
  • Pee out the sugar
    • Weight losing
    • But increases the risk of UTIs and thrush
166
Q

Motivational interviewing for diabetes

A

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)

167
Q

Explaining how to inject insulin

A
  • 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
168
Q

Purpose of AUSDRisk assessment tool

What does high risk mean?

A

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)

169
Q

Factors putting you at HIGH RISK of developing T2DM

A
  • 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
170
Q

Screening for diabetes in high risk population vs low risk population

A

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

171
Q

High risk CVD risk assessment score

A

> =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

172
Q

CVD risk assessment

A

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

173
Q

CVD risk assessment score - mod vs low risk management

A

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
174
Q

Assoc ft to ask on HX about back pain

A
  • 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)
175
Q

Indications for imaging in back pain

A

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
176
Q

Yellow flags - define and give examples

A

• 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)

177
Q

Risk assessment - depression

A
  • 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
178
Q

Management of depression in GP

A 
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
179
Q

Mental health care plan requirements

A 
Diagnosis of a mental health condition (not dementia, delirium, tobacco use disorder, mental retardation)
HOPC
Past history
Crisis plan
Outcome measure - K10
180
Q

How do you assess bleeding risk?

A

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

181
Q

CI to warfarin

A
  • 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)
182
Q

Medication Counselling Framework

A 
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

183
Q

Histopathology of coeliac disease: 3 features

A
  1. Villous atrophy and crypt hyperplasia
  2. Increased #s plasma cells and lymphocytes in LP
  3. Increased IELs (CD4 T cells)
184
Q

What sort of anaemia is associated w Coeliac disease?

A

Iron deficiency (microcytic)

or pernicious anaemia (B12, macrocytic)

185
Q

What part of bowel does coeliac mainly affect? What affect does this have on absorption?

A

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.

186
Q

Diagnosis of coeliac

A

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

187
Q

Potential complications of UC vs Crohns

A

Crohns:

  • Strictures
  • Fissures -> risk of perforation
  • Abscess
  • Fistulae
  • Perianal disease

US

  • toxic megacolon -> risk of perforation
  • incr risk colon cancer
188
Q

What are the main symptoms for Crohn’s vs UC

A

Crohns: abdominal cramps, diarrhoea, weight loss (malnutrition), fever

UC: rectal bleeding, urgency, tenesmus, abdominal cramps

189
Q

Extra colonic manifestations of Crohn’s vs UC

A

Crohns

  • perianal fistulae and skin tags
  • renal stones
  • cholelithiasis
  • oral ulcers

Both

  • rashes, erythema nodosum
  • arthritis, analysing spondylitis
  • uveitis, episcleritis
  • PSC
  • fatty liver
190
Q

Treatment of IBD

A

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
191
Q

What is the criteria for IBS?

A

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

192
Q

Where does diverticular disease usually affect? where is the pain generally felt?

A

Sigmoid colon

LLQ

193
Q

Management of diverticular disease

A

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.
194
Q

Causes of small vs large bowel obstruction

A

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

  1. Cancer
  2. Diverticulitis
  3. Volvulus

Rarer causes

  • Adhesions
  • Constipation
  • Volvulus (sigmoid or caecal)
195
Q

Gastritis - common causes of acute vs chronic

A 
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)
196
Q

Diagnosis of H pylori

A

Urea breath test
Serology and stool Ag test
Biopsy -> histology, rapid urease test

197
Q

Management of Peptic Ulcer Disease

A

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)
198
Q

What are the signs you get in the decompensation phase with CLD?

A

Encephalopathy -> drowsiness, metabolic flap

Jaundice

Ascitites + peripheral oedema

Leukonychia

Bruising/coagulopathy

Variceal bleeding

199
Q

What is the coagulopathy in CLD due to?

How would you measure this - what blood test?

A

Lack of coagulation factors (factor VIII) due to impoaired synthetic function of liver

Low platelet count due to splenomegaly from portal HTN

-INR

200
Q

Clinical features of acute viral hepatitis

A

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
201
Q

treatment biliary colic vs acute cholecystitis

A

Bilairy colic: analgesia and rehydration with elective cholecystecomy

Acute cholecystitis:

  • admit, hydrate, NPO, NG tube, analgesics
  • cefazolin
  • cholecystectomy early
202
Q

where does most pancreatic cancer occur (what part of hte pancreas?) and how does it manifest clinically?

A

Head of the pancreas in 70%
- Systemic SX, obstructive jaundice, vague constant mid-epigastric pain, painless jaundice, courvoisier’s sign
+/- palpable tumour mass

203
Q

DDX dysphagia

A

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)

204
Q

Indications for endoscopy with reflux

A 
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
205
Q

Complications with GORD

A
  • Esophagus stricture disease (scarring can lead to dysphagia)
    • Ulcer
    • Bleeding
    • Barrett’s esophagus and esophageal adenocarcinoma
206
Q

Pathophys Barrett’s oesophagus

A
  • 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
207
Q

1st vs 4th degree haemorrhoids

Relative tx

A

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

208
Q

Perianal bleeding (blood on toilet paper not mixed in)

Things to ask on bleeding

DDX

A 
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)
209
Q

Mx anal fissure

A

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)

210
Q
  • 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??

A

Mild type 1 vWF deficiency

Confirm via blood tests for:
vWF Ag levels
vWF activity or function tests

211
Q
  • X-linked inheritance
  • Characterised by joint bleeding! (often post-trauma)
  • Mildly elevated APTT

What is the provisional diagnosis and what test would confirm this?

A

Mild Type Haemophilia

Confirm via blood tests for factors 8 (deficiency=Type A) and 9 (deficiency=Type B)
And/or genetic tests

212
Q
  • 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?

A

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
213
Q
  • 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 ?

A

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)

214
Q
  • 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?

A

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.

215
Q

Differentials for abnormal bleeding

A 
Haemophilia A or B
vWF disorder
Other factor deficiency
Platelet disorder (ITP, TTP etc)
Anticoag/antiplatelet drugs

DIC
CLD

216
Q

Causes microcytic anaemia

A

Iron deficiency (slow chronic bleed or nutrient deficiency)

Anaemia of chronic disease

Thalassaemia

217
Q

Causes normocytic anaemic

A

Hypoproliferative

  • leukaemia
  • aplastic anaemia
  • pure red cell aplasia

Hyperproliferative

  • haemmhorage/bleed
  • haemolytic anaemia (sickle cell, thalassaemia, spherocytosis, G6DP deficiency, haemolytic uraemia, DIC, TTP)
218
Q

Causes macrocytic anaemia

A

Megaloblastic
-B12/folate deficiency

Non-megaloblastic

  • cirrhosis, liver failure
  • alcoholism
  • myelodysplastic syndrome
  • congenital bone marrow failure syndrome
  • myeloproliferative disorders
  • myeloma
219
Q

DDX for petechiae/purpura/ecchymosis

A
  1. Thrombocytopenia
    - ITP
    - Secondary to meds, leukaemia, SLE, APL syndrome, vWF deficiency
  2. Vascular disorders
    - Senile purpura, HTN, Henoch Schonlein purpura
  3. Coagulation problem
    - DIC or Scurvey
  4. MENINGOCCOCEMIA
220
Q

HSP triad

A

purpura
arthritis
abdo pain

221
Q

Causes of B12 deficiency

A

Absorption of B12 requires gastric acid and IF

  1. Atrophic gastritis (autoimmune - autoantibodies targeting IF)
  2. Pancreatic failure
  3. Post-gastrectomy -lack IF
  4. Crohn’s or resection of ileum
  5. Coeliac
  6. Vegan diet
222
Q

What causes folate deficiency anaemia?

A

Alcoholics
Malnourished patients
Pregnancy

223
Q

What cells are affected by AML and CML?

A

erythrocytes, mast cells, thrombocytes (plt), basophils, neutrophils, eosinophils, macrophages and monocytes

224
Q

What cells are affected by ALL and CLL?

A

ALL - B cells, T cells, NK cells

CLL- B cells mostly

225
Q

What is myeloma?

A

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)

226
Q

SX of myeloma

A

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

227
Q

What is Lymphoma?

A

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)

228
Q

What is Leukaemia?

A

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.

229
Q

What is the protein in the urine from MM called?

A

Bence Jones protein (paraprotein M)

230
Q

Genetic causes of too much clotting

A 
Antiphospholipid syndrome
Antithrombin III def
Protein C or S def
Factor V leiden
Prothrombin gene mutation
231
Q

2 types of lymphoma and their classic features

A
  1. Non-hodgkin’s lymphoma
    - Mostly diffuse large B cell lymphoma (more aggressive but higher cure rates)
    - T cell forms @ 30%
  2. 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

232
Q

Blood and urine results for a patient w multiple myeloma

A

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

233
Q

DX, IX and MX:

Vertigo when rolling over in bed onto R side, passing within a minute

A

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

234
Q

What is vestibular neuritis?

A

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.

235
Q

Features of Meniere’s disease

A

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

236
Q

MX of Meziere’s disease

A

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
237
Q

DDX Vertigo and relative time frames

A
  1. BPPV: <1min duration
  2. Meniere’s disease: 30min-1 day duration
  3. Vestibular neuritis: days-weeks
  4. Acoustic neuroma (elderly patients, tinnitis more common presentation than vertigo)
238
Q

DDX dizziness (light-headedness)

A

Medical

  • Haem: anaemia
  • Heart: dysrhythmia
  • Endocrine: hypoglycaemia
  • Drugs: antihypertensives

Neurological:

  • MS
  • Migraine
239
Q

features of COPD

A

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

240
Q

migraine mx

A

Prophylaxis:
propanolol
amitryptinine

Acute - NSAID +/- triptan

241
Q

DDX fatigue

A 
Depression, anxiety, stress/lifestyle
OSA
Thyroid
DM
post-viral infx
Anaemia
Malignancy
Chronic disease: CCF, CLD, CRF
242
Q

Testing hearing

A

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
243
Q

Acoustic neuroma features

What CN are affected

A 
One sided hearing loss
Vertigo
Tinnitis
Nausea
Unilateral FACIAL WEAKNESS, tingling

(CN 5,7,8 affected)

244
Q

Who is eligible for the Zostavax?

What does it do

A

70-79 year olds for the prevention of shingles (herpes zoster) and post-herpetic neuralgia

245
Q

What do you have to be wary of with shingles involving the face?

MX of this

A

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

246
Q

Mx of post herpetic neuralgia

A

Commence tx early!!!
pain can last >1-4 months from initial onset of rash +/- other sensory sx

mx - neuropathic pain medications (pregabalin, gabapentin, amitryptiline)

247
Q

Side effects of beta blockers

A 
Bradycardia and hypotension
orthostatic hypotensive
Transient worsening of HF
Bronchospasm (Care w asthma)
Cold extremities - Exacerbate Reynolds
Dizziness
248
Q

Relative CI to betablockers

A

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)

MD3 (7 decks)

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