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Physician Associate Studies > Everything > Flashcards

Everything Flashcards

1
Q

Presentation of Hypercalcaemia

A

STONES, BONES, GROANS, MOANS
Bone pain
Kidney stones
Constipation, nausea vomiting
Fatigue, depression, psychosis

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2
Q

Management of Hypercalcaemia

A

IV fluids

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3
Q

Presentation of Hypocalcaemia

A

CATs go numb
Convulsions
Arrythmia
Tetany and carpopedal spasm
Paraesthesia- Tingling
Muscle cramps
Seizure
Teeth deformity

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4
Q

Management of Hypocalcaemia

A

A-E
10ml IV calcium gluconate
Oral calcium + vit D

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5
Q

Causes of Hypocalcaemia

A

Low PTH
- parathyroid destruction by surgery, metastases or amyloidosis
-autoimmune

High PTH
- vit D deficiency
- PTH resistance

Hyperventilation
Acute Pancreatitis

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6
Q

Risk factors for hypocalcaemia

A

Lack of vitamin D & magnesium
IBD
CKD

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7
Q

Causes of hypercalcaemia

A

Norm/eleeaved PTH
Primary/tertiary hyperparathyroidism
Lithium induced hyperparathyroidism
Familial hypocalciuric hypercalcaemia
Low PTH
Malignancy
Vit d intoxication
Thyrotoxicosis
Adrenal insufficiency

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8
Q

What is chronic bronchitis

A

An infection of the bronchi, causing inflammation and irritation. This causes more mucus production and therefore coughing. Chronic- daily productive cough >3/12 for 2 years in a row.
1 of 2 conditions of COPD

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9
Q

risk factors for chronic bronchitis

A

Smoking
Exposure to irritants- grain dust, textiles, ammonia, strong acids.
Reduced immune system

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10
Q

risk factors for chronic bronchitis

A

Smoking
Exposure to irritants- grain dust, textiles, ammonia, strong acids.
Reduced immune system

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11
Q

What is the difference between Gastric and Duodenal ulcers

A

Gastric ulcer- pain worsened by food/eating, may have vomiting/haematemesis, melena, epigastric pain
Duodenal ulcer- pain improved by food/eating, pain few hours after eating.

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12
Q

What is erythema infectiousum

A

Parvovirus B19, slapped cheek, fifths disease

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13
Q

What is erythema infectiousum management

A

Fade over 1-2 weeks
Fluids, rest analgesia
Not infectious once they have the rash.

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14
Q

What is a fibroadenoma

A

The most common benign growth in the breast (neoplasia). They are proliferations of stromal and epithelial tissue of the duct lobules. They have a low malignant potential.
Commonly called breast mice because they move around so much.

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15
Q

presentation of fibroadenoma

A

Highly mobile lesions
Well-defined and rubbery on palpation
Often <5cm diameter
Can be multiple and bilateral
Change in size during pregnancy or premenstrual.

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16
Q

What is a pneumothorax

A

Occurs when air gets into the pleural space, separating the lung from the chest wall. It can occur spontaneously, secondary to trauma, iatrogenically or due to lung pathology. The typical patient is a tall, thin, young man presenting with sudden SOB and pleuritic chest pain when playing sport.

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17
Q

Where is the triangle of safety for a chest drain

A

The5th intercostal space(or the inferior nipple line)
Themidaxillary line(or the lateral edge of thelatissimus dorsi)
Theanterior axillary line(or the lateral edge of thepectoralis major

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18
Q

signs of a tension pneumothorax

A

Tracheal deviation
Reduced air entry on affected side
Increased resonance to precussion
Tachycardia
hypotension

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19
Q

what is strabismus

A

Also called a squint, is there the eyes point in different directions

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20
Q

causes of strabismus

A

Idiopathic
Hydrocephalus
Cerebral palsy
Space occupying lesions- retinoblastoma
trauma

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21
Q

management of strabismus

A

Refer (surgery for the muscles before the age of 7). Medial and laterus rectus for esotropia and exotropia (free lateral, tighten medial).
Corrective glasses
Occlusion therapy for lazy eye- use patch or classes part time.
penalization therapy (deliberately blur good eye using atropine drops to force child to use other eye- 2nd choice to occlusion)
Botulinum toxin – injection can cause paralysis for 3 months and correct a squint

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22
Q

What is vasovagal syncope

A

It is a benign condition caused by activation of the PNS in response to certain emotional or environmental triggers. Typically they occur after standing for a prolonged period of time, by fasting, dehydration, being in crowded or excessively warm environments or following stressful events, like seeing blood and needles. These trigger a vasovagal reaction that consists of bradycardia, vasolidation of peripheral blood vessels- hypotension, which reduces the brains oxygen supply resulting in cerebral hypoperfusion and loss of consciousness

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23
Q

what is orthostatic hypotension

A

when they drop BP when changing from lying to standing. This occurs due to a delay in constriction of the lower body veins, which is needed to maintain adequate blood pressure when changing to the standing position. When the delay occurs, it is due to blood pooling in the veins of the leg, resulting in less blood returning to the heard- causing a drop in cardiac output and blood pressure.

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24
Q

what is eisenmenger syndrome?

A

in Atrial septal defect. A complication where pulmonary pressure > systemic pressure, resulting in a right to left shunt- cyanotic

25
Q

management of atrial septal defect

A

If small and asymptomatic, monitoring may be appropriate
Closed through transvenous catheter closure or open heart surgery.
Anticoagulants (aspirin, warfarin and NOACs- used to reduce stroke risk in ADULTS).

26
Q

signs of atrial septal defect

A

SOB
Difficulty feeding
Poor weight gain
Lower respiratory tract infections
Mid-systolic, crescendo decrescendo murmur, splitting S2 sound.

27
Q

complications of atrial septal defect

A

Paradoxical embolism (doesn’t go to lungs, goes through defect to brain)
AF/ atrial flutter
Pulmonary hypertension
Eisenmenger syndrome- where pulmonary pressure > systemic pressure, resulting in a right to left shunt- cyanotic

28
Q

what is atrial septal defect

A

A hole in the membrane that separates the atria. It is a congenital condition. The foramen ovale is present in fetal circulation and allows for unidirectional blood flow (which should shut and fuse at birth). Causes a left to right shunt (pressure). The pressure is higher on the left, which overloads the right with blood and if large can cause damage to the heart if left untreated.

29
Q

risk factors for atrial septal defect

A

Associated with foetal alcohol syndrome
More common in down syndrome children

30
Q

what are haemorrhoids

A

Distended/abnormally swollen blood vessels within the anal canal. They either present above the dentate line (internal) or below (external). The line is 2cm above the anal verge. 1st degree-4th degree piles
internal
Do not prolapse
Prolapse on straining/reduce spontaneously
Prolapse on straining /reduce manually
Permanently prolapsed/ cannot be reduced.
External- lie under perianal skin. Have sensory innervation so may be painful, may be visible

31
Q

risk factor for haemorrhoids

A

Constipation
Prolonged straining
Heavy lifting
Increased abdo pressure, e.g. pregnancy ascites, pelvic mass
Chronic cough
Age
Exercise

32
Q

management of haemorrhoids

A

Prevent and manage constipation- increase fluids, fibre intake and laxatives
Analgesia, topic anaesthetic, anusol, topical corticosteroid to reduce inflammation,
Rubber band ligation, infrared coagulation, injection sclerotherapy
Surgical- haemorrhoidectomy, stapled haemorrohoidectomy
REFER & admit
Extreme pain, external present within 72hr onset
Internal haemorrhoids which have prolapsed and become swollen, thrombosed
perianal sepsis
Refer non urgent assessment if:
3rd or 4th degree which are too large for non operative measures
Perianal haematoma if <24hrs
Combined internal and external H’s with severe symptoms
Thrombosed haemorrhoids when bleeding is problematic or chronic irritation/lead
Large skin tags

33
Q

What murmur would you hear for tricuspid stenosis

A

mid/late diastolic at the left sternal edge, heard best during inspiraiton

34
Q

what is tricuspid stenosis

A

Narrowing of the tricuspid valve (right atrium to right ventricle (deoxygenated blood flow)).
It commonly occurs as a late complication of acute rheumatic aortic /mitral disease

35
Q

management of an animal bite?

A

Irrigate wound
Consider tetanus immunization
Abx prophylaxis- co-amoxiclav x5d
(doxycycline + metronidazole for those with penicillin allergy)
Cat, human <3 day old human bites, dog bites to face foot or genitals.
Involve ortho or plastics if surgical debridement is required
If human- blood tests for Hep B/C/ HIV

36
Q

types of bowel ischaemia

A

Decreased blood flow to the gastrointestinal tract. It can be acute or chronic mesenteric ischaemia or colonic ischaemia. Acute mesenteric ischaemia can be divided into embolic, thrombotic and venous. Colonic is most common and has the best prognosis.

37
Q

explain the main blood supply to the stomach

A

Foregut (stomach, duodenum, biliary system, liver, pancreas, spleen) – coeliac artery
Midgut- distal duodenum to frist ½ transverse colon- superior mesenteric artery
Hindgut- second ½ of colon to recum- inferior mesenteric artery

38
Q

what is chronic mesenteric ischaemia, its presentation and management

A

AKA intestinal angina- is the result of narrowing of mesenteric blood vessles by atherosclerosis. Results in intermittent abdo pain when the blood supply cannot keep up with demand. central colicky abdo pain after eating (30 mins post, 1-2hr duration), weight loss (due to food avoidance), abdominal bruits.

CT Angiography

Reduce risk factors- smoking, diet
Secondary prevention- statin, antiplatelet
Revascularisation to improve blood flow- endovascular procedure (percutaneous mesenteric artery stenting) or open surgery

39
Q

what is acute mesenteric ischaemia, its presentation and management

A

Typically cause by rapid blockage in blood flow through the superior mesenteric artery. This is caused usually by a throbus in the arty blocking blood flow. AF is a risk factor as the thrombus from the LA mobiliszes down the aorta to the superior mesenteric artery where it becomes stuck and cuts of the blood supply. Over time ischaemia to the bowel will result in nectosis of bowel tissue and perforation.

non-specific abdo pain- can go into shock, peritonitis and sepsis

Contrast CT, bloods- raised lactate & metabolic acidosis

Remove or bypass thrombus- endovascular or open surgery

40
Q

what assessed ulcerative colitis severity and what markers are needed

A

Truelove and witts severity score
- #bowel movements per day
- blood in stool
- temperature
- pulse >90
- anaemia
- ESR

41
Q

70% of patients with Primary sclerosing cholangitis have which other condition?

A

Ulcerative colitis

42
Q

what is ulcerative colitis

A

the colon and rectum. NEVER goes to anus or past caecum. Caused by environmental triggers in genetically susceptible people.
Most common form of IBD (UC or Crohn’s). It is relapsing-remitting. A severe exacerbation may be life threatening- worry about toxic megacolon.

43
Q

presentation of ulcerative colitis

A

Diarrhoea- often bloody
PR bleed
Increased faecal frequency and urgency Tenesmus
Abdominal Pain- left lower quadrant
Weight loss
Pallor, clubbing
Abdominal distention, tenderness or mass
Extra-intestinal manifestations
Aphthous ulcers, erythema nodosum, VTE, metabolic bone disease, episcleritis

44
Q

Investigations for ulcerative colitis

A

Truelove & witt severity
Bloods- FBC, CRP/ESR, TFT, kidney & LFT, U&E, ferritin, vit d, b12, TTGT, TPMT
Faecal calprotectin (<59 is normal)
Stool saple MC&S
Endoscopy- OGD and colonoscopy (pseudopolyp) w possibly biopsy.
Abdo XR- mural thickening
CT if toxic megacolon concern

45
Q

Management of ulcerative colitis?

A

Mild-mod – 1st line mesalazine, 2nd line corticosteroids
Severe – IV hydrocortisone, 2nd line –surgery- colectomy
Conservative- assess disease impact, annual bloods, assess osteoporosis risk, raise awareness for colorectal cancer surveillance
Remission- mesalazine, thiopurine

46
Q

complications of ulcerative colitis

A

Psychological impact
Toxic megacolon
Bowel obstruction
Bowel perforation
Intestinal stricture
Fistula
Anaemia
Malnutrition
Colorectal cancer- surveillance screening
pouchitis

47
Q

what is crohn’s

A

A form of IBD that can affect anywhere from the mouth to the anus in a discontinuous pattern (skip lesions). Inflammation is transmural, producing deep ulcers and fissures (cobblestone). It is not continuous, forming skip lesions. Relapsing-remitting.

48
Q

signs of crohn’s

A

Abdominal pain (colicky)
Diarrhoea
Fever
RIF pain

Weight loss
Clubbing
Apthous mouth ulcer
Strictures
Fistula
Anaemia
Erythema nodosum,anterior uveitis

49
Q

Investigation & management of crohn’s

A

Bloods (FBC (low HB., high platelet, high WCC) , U&E, LFT (low alb), high ESR, CRP
Stool MC&S (exclude infective colitis)
Faecal calprotectin
AXR-
Endoscopy (colonoscopy) and biopsy for definitive diagnosis – cobblestone appearance

Stress, stop nsaids
Induce remission
Steroid for acute exacerbations – oral prednisolone 40mg x7 days (then reduce)
Severe Flare- iv hydrocortisone
5-asa analogue- decrease the frequency of relapse in mild to moderate disease
Immunosupressants- azathioprine, methotrexate
Anti-TNFa agents – infliximab, adalimubab

50
Q

management of stable angina

A

Modify risk factors- stop smoking , exercise, weight loss, HTN control, statins.

Immediate symptomatic relief
GTN – glyceril trinitrate
causes vasolidation and helps to relieve symptoms. GTN can be repeated after 5 minutes.

Beta blocker- bisoprolol 5,g OD or CCB (amlodipine 5mg)
Aspirin 75mg OD
Atorvastain 80mg

PCI with coronary angioplast is offered to patients with proximal or extensive disease on CT coronary angiography. This involves putting a catheter into patients brachial or femoral artery, feeding up to coronary artery under xray and injecting contrast. Treated with balloon dilation and stent.
CABG with severe stenosis

51
Q

what is stable angina

A

A narrowing of the coronary arteries reduces blood flow to the myocardium. During exercise there is higher demand and therefore insufficient supply of blood to meet it. This causes angina. It is stable when relieved by rest of GTN.

52
Q

stress incontinence presentation and management

A

The loss of control of urination.
Can be stress or urge predominant
Stress- weakens of the pelvic floor and sphincter muscles. Allows urine to leak at times of increased pressure on the bladder
leakage When laughing, coughing or surprised

Investigations
Hx- caffeine, ETOH, med, BMI (ask frequency, nighttime urination and use of pads/clothes change
Bimanual Examine- prolapse, vaginitis, masses, urethral diverticulum
Bladder diary
Urine dipstick
Post-void residual bladder volume

Management
Avoid caffeine, diuretic, excessive fluid, kg loss
1st line – pelvic floor exercise (8 contractions TD for 3 months)
2nd- surgical- retropubic- mid urethral tape (TVT tension-free vaginal tape)
3rd- dulpxetine (if not surgical candidate)

53
Q

urge incontinence presentation and management

A

The loss of control of urination.
Can be stress or urge predominant
Urge- is caused by overactivity of the detrusor muscle of the bladder.

Sudden urge to pass urine
Not reaching bathroom in time
Conscious about having access to a toilet and may avoid places without access (QoL)

Investigations
Hx- caffeine, ETOH, med, BMI (ask frequency, nighttime urination and use of pads/clothes change
Bimanual Examine- prolapse, vaginitis, masses, urethral diverticulum
Bladder diary
Urine dipstick
Post-void residual bladder volume

Management
Bladder retraining 6w
Bladder stabilizing drugs; 1- antimuscarinic (Oxybutynin, tolterodine, darifenacin)

54
Q

FBO in eye management

A

high velocity then refer for slit lamp assessment- risk of penetration
If low velocity/ no risky hx then attempt removal if confident
Else refer
use topical anaesthetic and the tip of a sterile needle at an oblique angle
DONT USE COTTON BUD

Topical prophylactic antibiotic (chloramphenicol)
Oral analgesia

55
Q

pericarditis diagnosis and management

A

Inflammation of the pericardium. Can be idiopathic or secondary to viruses, bacteria, fungi, MI, drugs or other reasons.

Central chest pain
Worse on inspiration or lying flat
SOB
Possible pericardial rub: due to friction between the pericardial layers, typically loudest at the left lower sternal border, best heard with the patient leaning forward

ECG- tachycardia, saddle ST
bloods

NSAID’s (with PPI)- paracetamol
Antibiotics- if caused by bacterial infection.
Pericardial window surgery if symptoms persist.

56
Q

what is polyarteritis nodosa

A

A rare disorder characterized by widespread inflammation, weakening and damage to small and medium-sized arteries. It can affect vessels in any organ or system including kidneys, heart, intestines, muscles. This can result in hypertension, aneurysms, thrombus or necrosis.
Cause unknown but an attack can be triggered by drugs, vaccines or reaction to infection e.g. strep, stap, hep b.

57
Q

breast abscess & management

A

A collection of pus within the breast lined with granulation tissue, most commonly developing from acute mastitis.

Hx of recent mastitis or prior breast abscess
Fever &/or general malaise
A painful, swollen lump in the breast with redness and erythema

Management
Urgent referral to secondary care for confirmation of the diagnosis and management

Drainage of the abscess (USS guided needle aspiration or surgical drainage)
Culture of fluid from the abscess (which will guide the choice of antibiotic)

Women can still breastfeed. If painful or infant refuses they can express milk by hand or pump until able to resume as normal.

58
Q

management of OA

A

Conservative
exercise, weight loss if relevant, heat or cold packs, joint supports, physio or occupational therapists
Medical
Analgesia- paracetamol,
topical NSAIDs/capsaicin (if ineffective codine or oral NSAID + PPI (omepreazole).
Steroid injections
Surgical
Joint replacement/fusion if severe.

Physician Associate Studies (4 decks)

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