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Medicine year 4 CDM > GP 2 > Flashcards

GP 2 Flashcards

1
Q

Dementia: signs and symptoms

A
  • Memory loss: recent information
  • Difficulty with familiar tasks i.e. cooking
  • Language: struggling to find the right word
  • Disorientation
  • Poor judgement
  • Changes in mood and behaviour: irritability, anxiety or depression
  • Withdrawing from social activity
  • Personality change
  • Difficulty in abstract thinking
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2
Q

Dementia: diagnosis

A
  • Assess cognitive decline with MMSE, MOCA, mini-cog, ACE-III
  • Blood test: FBC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV
  • MRI or CT head
  • If dementia is suspected refer to specialist dementia diagnostic service (memory clinic)
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3
Q

Assessing risk in patients with dementia ‘HOW SAFE’

A
  • HOme safety (gas)
  • Wandering
  • Self neglect
  • Abuse
  • Falls
  • Eating
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4
Q

General management of dementia

A
  • Lifestyle – patients encourage to stay physically and mentally active. Written information for all patients.
  • Social – adult social services, occupational therapy assessment. May need support at home
  • Planning ahead: lasting power of attorney, end of life care, advanced decisions
  • Psychological – group stimulation therapy.
  • Pharmacological – e.g. donepezil (mild-moderate AD), memantine (severe AD), acetylcholinesterase inhibitors for LBD, optimising CV profile in VD.
  • BPSD in dementia – where delirium has been ruled out. 6-12/52 low-dose risperidone
  • Antipsychotics are last line and contraindicated in LBD and PD
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5
Q

Vascular dementia definition

A

caused by ischaemic or haemorrhage cerebrovascular disease, with progressive stepwise cognitive deterioration over months or years. Typical presentations are stroke-related vascular disease, subcortical vasculardementia (small vessel disease), and mixeddementia (combination of Alzheimers and vascular). Second most common type of dementia.

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6
Q

Vascular dementia presentation

A

less impairment in episodic memory and more in visual skills, semantic memory and executive functioning

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7
Q

Criteria for vascular dementia

A
  • the onset of dementia within three months following a recognised stroke
  • an abrupt deterioration in cognitive functions
  • fluctuating, stepwise progression of cognitive deficits
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8
Q

Diagnosis of vascular dementia

A
  • A comprehensive history and physical examination
  • Formal screen forcognitive impairement
  • Medical review to exclude medication cause of cognitive decline
  • MRI scan - may show infarcts and extensive white matter changes
  • Imaging: in MRI head there is extensive white matter change and infarcts evident
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9
Q

Management of vascular dementia

A
  • Reduction of cardiovascular risk factors like hypertension, diabetes and smoking
  • Cognitive stimulation programmes; music and art therapy
  • Symptomatic treatment, including cognitive enhancers such as cholinesterase inhibitors or memantine - if there is evidence of co-existent AD, Parkinson’sdementia, ordementia with Lewy bodies.
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9
Q

Lewy body dementia pathophysiology

A

alpha synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas). Accounts for 20% of dementia (third most common)

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9
Q

Lewy body dementia features

A
  • progressivecognitive impairement: in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
  • cognition may be fluctuating, develops 1 year before parkinsonism
  • parkinsonism
  • visualhallucinations: classically of small creature, children (other features such as delusions and non-visual hallucinations may also be seen)
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10
Q

Lewy body dementia: investigations and management

A
  • Investigations: clinical diagnosis but can use DAT scan
  • Management: use acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine
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11
Q

Alzheimers pathophysiology

A

Chronic, neurodegenerative disorder caused by the accumulation of (alpha-beta) amyloid plaques and tau tangles in the brain. As it develops it can lead to neuronal loss and brain atrophy. Causes defecit in the neurotransmitter acetylcholine and neuroinflammation. Most common cause of dementia

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12
Q

Alzheimers: clinical features

A
  • Memory impairment: early on, recalling recent events
  • Language impairment, difficulties in activities of daily living, executive dysfunction, behavioural changes (agitation), disorientation, psychological (hallucination)
  • MRI: brain atrophy and amyloid plaques. May be predominantly in the medial temporal lobe
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13
Q

Alzheimers medical management

A
  • The cholinesterase inhibitors rivastigamine, galantamine, and donpezil in mild-moderatedementia
  • NMDA inhibitor memantine in severedementia(as classified using the MMSE score: severe: <10; moderate: 10-20; mild: 21-26/30.
  • If evidence of behavioral and psychological symptoms ofdementia(BPSD), low-dose risperidone may be started
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14
Q

Fronto temporal dementia

A
  • Definition: Neurodegenerative disorder due to atrophy of the frontal and/or temporal lobes of the brain
  • One of the most common forms of early onset dementia but rare overall
  • Lots of different causes: some are familial
  • Can be caused by Pick’s disease: due to ‘Pick’s bodies’ accumulation of TAU protein within neurons (familial)
  • Prognosis is 7-13 years
  • Starting age 40-60
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15
Q

Fronto temporal dementia presentation

A
  • Personality changes: often exhibit disinhibited behaviour and apathy early on
  • Language impairment
  • Cognitive decline: memory is relatively preserved early on, executive function is relatively impaired
  • Motor abnormalities: may get muscle weakness and dysarthria
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16
Q

Fronto temporal dementia investigations

A
  • MRI or CT: shows atrophy of the frontal and/or temporal lobes. Specifically MRI can show focal gyral atrophy and knife blade appearance
  • Genetic testing: if you suspect an inherited form of FTD
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17
Q

Fronto temporal dementia management

A
  • Counselling, Behaviour modification strategies, caregiver support. Discuss driving- have to inform DVLA of diagnosis
  • Referral to specialist psychiatry or neurology services
  • SSRI’s and antipsychotics: help control behavioural symptoms. Benzos if acute
  • Don’t use Memantine and cholinesterase inhibitors
  • Supportive: SALT and occupational therapy
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18
Q

Classification of diverticular disease

A
  • Diverticular disease: conditions related to the presence of diverticula which are small, bulging pouches that can form in the lining of the digestive system most commonly in the sigmoid colon
  • Diverticulosis: the simple presence of diverticula, may be asymptomatic
  • Diverticulitis: when the diverticula become inflamed or infected.
19
Q

Risk factors and pathophysiology of diverticular disease

A
  • Risk factors: >50 with poor diet (low fibre), genetics, obesity, NDAID’s and opioids
  • Increased intraluminal pressure within the colon causes herniation of the mucosa and submucosa at points of weakness. These can retain faecal matter and become infected causing diverticulitis
20
Q

Symptoms of diverticular disease/diverticulitis

A
  • Diverticular disease: constipation, left lower quadrant pain, rectal bleeding, change in bowel habit
  • Diverticulitis: LIF pain, fever, N+V, pyrexia, diffuse abdo pain suggestive of peritonitis, leukocytosis, tachycardia, guarding
21
Q

Diverticular disease investigations

A
  • Abdominal imaging: CT scan (gold standard) or US
  • Bloods: FBC (leukocytosis), U&E, LFT
  • Colonoscopy/endoscopy: avoid during acute phase but perform 6 weeks after to confirm diagnosis
22
Q

Management of diverticular disease

A
  • Asymptomatic diverticulosis: no treatment needed
  • Symptomatic diverticular disease: increase dietary fibre and water
  • May need laxatives: use bulk forming (ispaghula husk) and avoid stimulant laxatives
23
Q

Management of diverticulitis

A
  • Oral antibiotics: 7 days co-amoxiclav, if severe IV piperacillin-tazobactam.
  • Give oral paracetamol.
  • Take clear liquids and avoid solid food till symptoms improve
24
Q

Treatment for severe diverticulitis

A
  • Unresponsive to abs, perforation, stricture or obstruction: may need surgical interventions. Abscess can be drained under CT
  • Recurrent diverticulitis: consideration for elective colectomy (primary resection with anastomosis or Hartmanns)
  • Acute rectal bleeding: Haemodynamic stabilisation, endoscopic haemostasis.
  • Prophylaxis: high fibre diet and mesalazine after the acute phase
25
Q

Complications of diverticular disease

A
  • Abscess (short term): bowel rest, broad spectrum abx +/- CT guided percutaneous drainage if medical management fails
  • Perforation (short term): surgical emergency suspected in peritonitis, will see free air on abdo x-ray, urgent explorative laparotomy
  • Fistula formation (long term): present with pneumaturia, faecaluria, and recurrent UTIs. Diagnosed with cystoscopy or cystography and require surgical repair. Colovaginal, coloenteric, colouterine, and colourethral fistulas may also occur.
  • Fibrosis: cause strictures and LBO
26
Q

Colonic diverticular disease

A
  • When the diverticular become inflamed and bleed
  • Painless rectal bleeding (mild to severe)
  • Inv: colonoscopy within 24hr with therapeutic interventions like endoscopic clipping or thermal coagulation
  • If colonoscopy not feasible CT angiography or surgery may be necessary (segmental colectomy)
  • Avoid NSAIDs and anticoagulants
27
Q

GORD

A
  • Clinical diagnosis due to symptoms of dyspepsia, heartburn or acid reflux
  • Other symptoms: Epigastric pain, Nausea, bloating, belching, nocturnal cough, hoarse voice
  • Due to reflux of gastric contents into the oesophagus due to a defective lower oesophagus sphincter
  • Risk factors: obesity, chronic alcohol use, smoking, spicy food, coffee
  • Complications: oesophageal ulcer, oesophageal stricture, Barretts oesophagus, Oesophageal cancer
28
Q

Criteria for reflux symptoms and OGD

A
  • Age >55 years
  • Symptoms >4 weeks
  • Dysphagia
  • Persistent symptomsdespite treatment
  • Relapsing symptoms
  • Weight loss
  • Excessivevomiting
  • GI bleeding
29
Q

GORD management

A
  • Lifestyle: weight loss, dietary change, stop smoking, elevation of the head at night, avoidance of late night eating
  • PPI: if patient <40 with no red flags. Give for 4-8 weeks with lifestyle change. If symptoms return, step PPI dosage down to the lowest level which relieves symptoms
  • Offer H2 receptor antagonist therapy if inadequate response to PPI
  • Dont give PPI yet if need urgent OGD
  • Antacids for symptom relief
  • Anti-reflux surgery for symptomatic relief (Nissen fundoplication): diagnosis must be confirmed by endoscopy and cant take the meds
30
Q

Haemorrhoids definition and risk factors

A

Definition: where the vascular cushions within the anal canal abnormally expand and protrude outside the anal canal

Risk factors: age, pregnancy, constipation, obesity, chronic cough, weightlifting

31
Q

Haemorrhoids signs and symptoms

A
  • Bright red blood: on defecation or wiping
  • Absence of pain
  • Anal pruritis
  • A palpable or protruding mass in the anal region during examination
  • Investigation: PR exam
32
Q

Types of haemorrhoids

A
  • External: originate below the dentate line, prone to thrombosis may be painful. Visible on inspection as swelling covered in mucosa
  • Internal: originate above the dentate line, do not generally cause pain. May be felt on PR (although generally difficult)
33
Q

Haemorrhoids: prolapse grades

A
  • Grade 1: do not prolapse out of the anal canal
  • Grade 2: prolapse on defecation but reduce spontaneously
  • Grade 3: can be manually reduced
  • Grade 4: cannot be reduced
34
Q

Management of haemorrhoids

A
  • Soften stools: increase dietary fibre and fluid intake
  • Grade 1: Conservative management, topical corticosteroids or anaesthetics to alleviate pruritus
  • Grade 2: Management may involve rubber band ligation (preferred), sclerotherapy, or infrared photocoagulation
  • Grade 3: Rubber band ligation
  • Grade 4: Surgical haemorrhoidectomy, Haemorrhoidal artery ligation
35
Q

Thrombosed haemorrhoids

A

strangulation at the base of the haemorrhoid, causing a clot in the haemorrhoid. Painful, purple protrusions. Conservativemeasures such as ice packs,laxatives, and lidocaine gel are first-line treatments. If these measures fail, haemorrhoidectomy may be required.

36
Q

Head lice definition and risk factors

A

Head lice: small wingless insects that infect the hair and scalp feeding on human blood. Known as Pediculus humanus capitis and attach their eggs to hair shafts.

Risk factors: school age kids, poor personal hygiene, close contact with infected individuals, sharing combs, hats or pillows, long hair

37
Q

Head lice: signs and symptoms

A
  • Persistent itching of the scalp, neck, and behind the ears.
  • Presence of nits attached to hair shafts near the scalp.
  • Small red spots on the scalp or neck
  • Adult lice crawling on the scalp or hair.
  • Sores or skin infections due to scratching
  • Clinical diagnosis, schools may have routine screening programmes. Can use dermatoscope if uncertain
38
Q

Headlice management

A
  • Wet coming: after washing hair with conditioner still in, the hair is combed with fine toothed comb and checked for lice after each stroke. Repeat every 3-4 days for 2 weeks
  • Medication: malathion, permethrin, dimeticone 4% lotion
  • Chemical insecticides like Malathion 0.5% liquid
  • Avoid head to head contact and sharing combs, wash linen and clothes used in last 48 hours
39
Q

Hiatus hernia: definition and risk factors

A

Definition: where the abdominal contents protrude through an enlarged oesophageal hiatus in the diaphragm

Risk factors: obesity, prior hiatal surgery, chronic cough, pregnancy, ascites, smoking

40
Q

Types of hiatus hernia

A
  • Sliding hiatal hernia (80%): the gastro-oesophageal junction slides into the chest. Causes a less competent sphincter and acid reflux. Treatment is similar to GORD
  • Rolling hiatal hernia (20%): the gastro-oesophageal junction stays in the abdomen but part of the stomach protrudes into the chest alongside the oesophagus. Needs more urgent treatment can cause ischaemia and necrosis
41
Q

Hiatus hernia symptoms and investigations

A

Symptoms: Heartburn, Dysphagia, Regurgitation, SOB, Chronic cough, oesophagitis and chest pain

Hiatus hernia investigations

  • Barium swallows(upper GI series): first line
  • Endoscopy: gold standard (can take biopsies)
  • Oesophageal manometry, Ph monitoring
42
Q

Hiatus hernia: management

A
  • Weight loss, elevate the head of the bed, smoking cessation
  • Avoid large meals, alcohol, acidic food and eating before bedtime
  • Medical: PPI for 4-8 weeks before assessing response, Second line H2 receptor antagonist
  • Surgical management: Nissen fundoplication
43
Q

Infective mononucleosis

A
  • Also called glandular fever, caused by EBV (human herpesvirus 4)
  • Tends to affect young adults
  • Transmitted through infected saliva
  • Symptoms: fever, general malaise, sore throat, transient macular rash, lymphadenopathy, mild hepatosplenomegaly
44
Q

Potential serious features of infective monucleosis

A
  • Palatal petechiae
  • Splenomegaly- occurs in around 50% of patients and may rarely predispose to splenic rupture
  • Hepatitis, transient rise in ALT
  • Lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
  • Thrombocytopaenia
  • Haemolytic anaemia secondary to cold agglutins (IgM)
  • Chronic fatigue
  • A maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis
45
Q
A
46
Q

Investigations for infective mononucleosis

A
  • FBC: elevated leukocytes
  • Monospot test: do in second week of illness, if negative retest in 5-7 days
  • EBV viral serology: done if patient is <12, immunocompromised or if monospot is still negative but clinical suspicion
  • Abdo US: if assessing splenomegaly
  • HIV test
47
Q

Management for infective mononucleosis

A
  • Conservative: illness tends to resolve within 2-4 weeks without intervention
  • Analgesia, Hydration
  • Avoid alcohol (worsen symptoms) and avoid amoxicillin and ampicillin (cause itchy maculopapular rash)
  • Contact sport: avoid for 3 weeks (risk of splenic trauma)
  • Rare complications: haemophagocytic lymphohistiocytosis,aplastic anaemia, acuteliver failureand upper airway obstruction

Medicine year 4 CDM (44 decks)

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