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3A REVISION > GP 2 > Flashcards

GP 2 Flashcards

1
Q

What is dyspepsia?

A

Indigestion - upper abdo symptoms such as heartburn/acidity/pain/discomfort/nausea/bloating

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2
Q

Symptoms of dyspepsia?

A

Epigastric pain often related to hunger, specific foods, or time of day
Bloating, fullness, heartburn

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3
Q

ALARMS symptoms in dyspepsia?

A 
Anaemia
Loss of weight
Anorexia
Recent onset/progressive
Melaena/haematemesis
Swallowing difficulty

> 55 years

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4
Q

If >55 or ALARMS signs what is management?

A

Upper GI endoscopy

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5
Q

If <55 or no ALARMS signs what is management?

A

Lifestyle advice, ITC antacids, review

If no improvement test for H.pylori - Carbon 13 breath test

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6
Q

Management if no H.pylori present and still symptoms?

A

PPI (omeprazole) or H2 blockers (ranitidine) for 4 weeks

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7
Q

Management if H.pylori present?

A

Omeprazole AND amoxicillin (or metronidazole) AND clarithromycin

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8
Q

What is GORD?

A

Gastrooesophageal reflux disorder

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9
Q

Pathophysiology of GORD?

A

Reflux of stomach contents causes symptoms i.e. heartburn or complications i.e. oesophagitis

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10
Q

Causes of GORD? (6)

A 
Lower oesophageal sphincter hypotension
Hiatus hernia
Loss of gastric peristalsis/slow emptying
Obesity
Acid hypersecretion
Smoking, alcohol, overeating
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11
Q

Symptoms of GORD? (5)

A 
Heartburn - burning retrosternal discomfort, worse on lying or after big meal
Acid/bile/water regurgitation
Belching
Painful swallowing
Can cause cough, hoarse voice
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12
Q

Complications of GORD?

A 
Oesophagitis
Benign stricture
Ulcers
Iron deficiency
Metaplasia - barrett's oesophagus (squamous to columnar change)
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13
Q

Investigations in GORD? (4)

A

Endoscopy - esp if ALARMS, refractive, palpable mass, persistent vomiting
Barium swallow may show hiatus hernia (gastro-oesophageal junction slides into chest and sphincter is less competent)
Oesophageal pH monitoring
Bloods - FBC for anaemia

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14
Q

Lifestyle changes for GORD? (6)

A

Raise bed head
Weight loss
Stop smoking
Smaller, regular meals
Avoid - hot drinks, fizzy, alcohol, citrus fruits, spicy foods, coffee, chocolate, eating before bed
Avoid NSAIDs or other gastric damaging drugs

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15
Q

Medications for GORD?

A

Antacids - magnesium trisilicate mixture
Alginates - Gaviscon
Proton pump inhibitor - lansoprazole
H2 blocker - ranitidine

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16
Q

Surgery for GORD?

A

Nissen fundoplication to increase LOS pressure

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17
Q

How do antacid containing alginates work?

A

Form a foam raft over gastric contents to reduce reflux

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18
Q

How do PPIs work?

A

Inhibits the membrane enzyme H+/K+ ATPase to inhibit gastric acid secretion

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19
Q

CI/SEs of PPIs

A

CI: can increase risk of fractures in elderly, GI infections, may mask gastric cancer symptoms
SE: abdo pain, constipation, dizziness

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20
Q

How does ranitidine work?

A

Blocks the H2 (histamine) receptors, stops cells from producing acid

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21
Q

What is IBS?

A

Irritable bowel syndrome - mixed group of abdominal symptoms for which no organic cause can be found

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22
Q

Cause of IBS?

A

Most due to disorders of intestinal motility or enhanced visceral perception

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23
Q

Diagnosis of IBS?

A 
Abdominal pain/discomfort relieved by defecation OR associated with altered stool form/frequency
AND 2 of:
Urgency
Incomplete evacuation
Abdominal bloating/distension
Mucous PR
Worse symptoms after food

Chronic >6 months

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24
Q

What can exacerbate IBS?

A

Menstruation
Stress
Gastroenteritis

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25
Q

Signs of IBS?

A

May have generalised abdo tenderness

Pt is younger woman

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26
Q

Tests for IBS?

A

Exclude other diagnoses - FBC, ESR, CRP, LFT, coeliac serology
Colonoscopy if unsure
May need Ca125 to exclude ovarian Ca

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27
Q

Management of IBS? (4)

A

Healthy diet - fibre, lactose, starch, caffeine, alcohol may worsen
Bisacodyl laxative
Loperamide for diarrhoea
Antispasmodics - mebeverine

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28
Q

What is coeliac disease?

A

T cell mediated autoimmune disease of the small bowel

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29
Q

Pathophysiology of coeliac disease?

A

Prolamin intolerance i.e. gliadin (gluten proteins) causes villous atrophy and malabsorption

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30
Q

Associated conditions with coeliac?

A 
HLA DQ9/8 - other autoimmune disease
Dermatitis herpetiformis (severe itching, red raised patches that often blister)
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31
Q

Symptoms of coeliac disease? (11)

A 
Diarrhoea
Stinking stools/steatorrhoea
Abdominal pain
Bloating
Nausea, vomiting
Apthous ulcers
Angular stomatitis
Weight loss
Fatigue
Osteomalacia
Failure to thrive
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32
Q

Diagnosis/investigation of coeliac disease? (4)

A

Bloods - low Hb, low B12, low ferritin
Antibodies - alpha gliadin, tissue transglutaminase, IgA anti-endomysial (most specific)
Endoscopy and biopsy
SYMPTOMS/SIGNS REVERSE ON GLUTEN FREE DIET

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33
Q

What is seen on endoscopy/biopsy in coeliac?

A

Duodenal biopsy shows subtotal VILLOUS ATROPHY, INTRA EPITHELIAL WBCs, CRYPT HYPERPLASIA

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34
Q

Treatment of coeliac disease? (3)

A

Lifelong gluten free diet
Can prescribe gluten free bread, pasta, flour
Verify diet by anti-endomysial antibody monitoring

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35
Q

Complications of coeliac disease? (6)

A 
Anaemia
T cell lymphoma
Malignancy - gastric, oesophageal, bladder
Myopathies
Neuropathies
Osteoporosis
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36
Q

What is ulcerative colitis?

A

Relapsing and remitting inflammatory disorder of the colonic mucosa

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37
Q

Distribution of UC?

A

Just the rectum (proctitis) or extend to part of the sigmoid or whole colon - never proximal to ileocaecal valve

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38
Q

Cause of UC?

A

Unknown. Some genetic risk

Smoking is protective

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39
Q

Pathology of UC?

A

Haemorrhagic granular colonic MUCOSA, possibly with pseudopolyps formed by inflammation
Punctate ulcers into lamina propria but not usually transmural

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40
Q

Symptoms of UC? (5)

A 
Episodic/chronic diarrhoea possibly with blood and mucus
Crampy abdo pain
Bowel frequency
Urgency
Fever, malaise, weight loss
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41
Q

Signs of UC?

A

If acute may be fever, tachycardia, tender abdomen

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42
Q

Extraintestinal signs of UC? (6)

A 
Clubbing
Apthous ulcers
Erythema nodosum
Conjunctivitis, episcleritis, iritis
Large joint arthritis
Ankylosing spondylitis
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43
Q

Tests for UC?

A

Blood - FBC, U+E, LFT, ESR, CRP, cultures
Stool MC+S
Abdo XR
Colonoscopy and biopsy

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44
Q

What is seen on abdo XR in UC?

A

Mucosal thickening and colonic dilatation

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45
Q

What is seen in colonoscopy biopsy in UC? (5)

A 
Inflammatory infiltrate
Goblet cell depletion
Glandular distortion
Mucosal ulcers
Crypt abscesses
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46
Q

Complications of UC? (5)

A 
Perforation
Haemorrhage
Toxic colon dilatation
Venous thrombosis
Colonic cancer
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47
Q

How is mild UC treated? (<4 stools, small bleeding) (2)

A

5-aminosalicylic acid (5-ASAs) - sulfasalazine for remission induction/maintenance
Prednisolone low dose 2 wks helps remission induction

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48
Q

How is moderate UC treated? (4-6 stools, moderate bleeding) (3)

A

Oral prednisolone high dose for 2 weeks

Lower dose for 4 weeks with sulfasalazine and steroid enemas

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49
Q

How is severe UC treated? (>6 stools, unwell, large bleeding) (5)

A

ADMIT for NBM and fluids
Hydrocortisone IV
Rectal hydrocortisone
Daily testing, consider transfusion

Transfer to prednisolone high dose and sulfasalazine if improving

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50
Q

How is severe UC that is not improving treated? (2)

A

Rescue therapy - ciclosporin or infliximab

Surgery - colectomy

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51
Q

What is Crohn’s disease?

A

Chronic inflammatory GI disease

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52
Q

Pathology of Crohn’s?

A

TRANSMURAL granulomatous inflammation affecting the GI tract from mouth to anus
Skip lesions - unaffected areas between disease (UC is continuous)

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53
Q

Cause of Crohn’s?

A

Unknown. Smoking increases risk, genetics

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54
Q

Symptoms of Crohns? (5)

A 
Diarrhoea/urgency
Abdo pain
Weight loss/FTT
Fever, malaise, anorexia
Vomiting
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55
Q

Signs of Crohns?

A

Apthous ulcers
Abdo tenderness
Perianal abscesses/fistulae/SKIN TAGS
Anal strictures

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56
Q

Extraintestinal signs of Corhns? (5)

A 
Clubbing
Erythema nodosum 
Large joint arthritis
Ankylosing spondylitis
Conjunctivitis, episcleritis, iritis
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57
Q

Complications of Crohns? (7)

A 
Small bowel obstruction
Toxic dilatation - rarer than UC
Abscesses
Fistulae 
Perforation
Haemorrhage
Colon cancer
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58
Q

Tests for Crohns? (6)

A 
Bloods - FBC, ESR, CRP, U+E, LFT, ferritin, folate, B12
Stool MC+S
Colonoscopy and biopsy
Small bowel enema, barium enema
MRI to assess extent and fistulae
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59
Q

What is seen on colonoscopy and biopsy in Crohns? (6)

A 
Deep fissured ulcers - transmural
Skip lesions
Narrowed lumen
Inflammatory infiltrate
Granulomas with or without langhans giant cells
Lymphoid hyperplasia
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60
Q

How are mild attacks (systemically well) treated in Crohns?

A

Prednisolone high for 1 week, lower for 4 and wean off

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61
Q

How is severe Crohns treated?

A

ADMIT for NBM, fluids
IV hydrocortisone, rectal hydrocortisone
Metronidazole IV
Daily testing, consider transfusion

If improving transfer to oral prednisolone

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62
Q

How to treat severe Crohns that is not improving?

A

Infliximab, adalimumab

Surgery if refractive

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63
Q

Other drugs that may be given in Crohns? Useful in <50%

A

Azathioprine, methotrexate - steroid sparing

Sulfasalazine MAY work

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64
Q

How does sulfasalazine work? CI, SEs

A

Decreases inflammation, inhibits prostaglandin formation
SE: reversible infertility in men, rash, headache (rarely pancreatitis, hepatitis)
CI: asthma, risk of hepatic toxicity

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65
Q

How do infliximab/adalimumab work? CI, SEs

A

TNF alpha inhibitors, counter granuloma formation and WC infiltration
CI: sepsis, liver disease
SE: rash, infections

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66
Q

What is osteoarthritis?

A

Commonest joint condition.

Disease of synovial joints, usually primary but may be secondary i.e. to obesity

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67
Q

Structures involved in osteoarthritis?

A

The whole joint structure inc. cartilage, ligaments, capsule

Localised disease usually knee or hip

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68
Q

Pathogenesis of OA?

A

Loss of articular cartilage

Remodelling of underlying bone due to mechanical damage/inflammation/metabolic defect

69
Q

In whom is OA most common?

A

Females >50

70
Q

Symptoms of localised OA? (6)

A 
Usually KNEE or HIP pain on movement
Crepitus
Worse at end of day
Background pain at rest
Stiffness AFTER rest
Joint instability
71
Q

Symptoms of generalised OA? (7)

A 
Commonly DIP joints, thumb meta-carpals, knees
Heberden's nodes - DIP
Bouchards nodes - PIP
Joint tenderness
Derangement
Bony swelling
Decreased ROM
Synovitis
72
Q

Investigations in OA?

A

Bloods - ESR, CRP

XR/MRI

73
Q

What does XR show in OA?

A

Loss of joint space
Osteophytes
Subarticular sclerosis
Sunchondral cysts

74
Q

Management of OA? (6)

A

Exercise, weight loss
Analgesia - paracetamol, topical NSAIDs, codeine
Intra-articular steroid injections
MDT - Physio, OTs
Heat/cold packs, stretching
Surgery - joint replacement for hip or knee

75
Q

MDT advice to give in OA?

A 
Physio for exercises, splints
OT for aids i.e. walking stick
Chiropodist for foot care
Social worker for benefits, housing
Orthopaedics for surgery
76
Q

What is rheumatoid arthritis?

A

Most common disorder of connective tissue

77
Q

Cause of RA?

A

Immunological

Triggered by environmental factors in patients with a genetic predisposition

78
Q

How does RA present? (6)

A 
Commonly in middle aged females
Symmetrical small joint involvement - pain, stiffness, swelling, functional loss
EARLY MORNING STIFFNESS
Joint deformity and damage
Can be monoarthritis
Systemic - malaise, pain
79
Q

Signs of RA?

A

Predominantly peripheral joints
Joint effusions
Soft tissue swelling

80
Q

Investigations of RA? (3)

A

FBC - anaemia, ESR/CRP high
Rheumatoid factor and anti-CCP antibodies
XR

81
Q

What does XR show in RA?

A

Early - normal osteoporosis or soft tissue sweling

Later - loss of joint space, erosions, joint destruction

82
Q

Management of RA? (4)

A

MDT - physio, OT, surgery, nurse
Exercise and splints
NSAIDs and paracetamol
Corticosteroid joint injections
DMARDS - methotrexate, sulfasalazine, rituximab
Surgery - joint fusion/excision/replacement

83
Q

Complications of RA? (5)

A 
Disability
Depression
Osteoporosis
Infections
Amyloidosis
84
Q

Features of RA in the hands? (4)

A 
Ulnar deviation of the fingers
Z deformity of thumb
Swan neck (extended PIP, flexed DIP) and boutonniere (flexed PIP, extended MCP and DIP) deformities of the fingers
85
Q

Non joint features of RA?(6)

A 
Rheumatoid nodules on forearms
Vasculitis
Sjogrens, episcleritis, scleritis
Mononeuritis/peripheral neuropathy
Pleural effusions, lung nodules
Pericarditis
86
Q

Indications of warfarin? (3)

A

Prophylaxis of embolisation in rheumatic heart disease and atrial fibrillation,
Prophylaxis after insertion of prosthetic heart valve,
Prophylaxis and treatment of venous thrombosis and pulmonary embolism, TIAs

87
Q

Target INR for warfarin?

A

2-3 (2.5)

If recurrent VTE, 3.5 (higher dose warfarin)

88
Q

Length of warfarin treatment after VTE?

A

Provoked - 3 months

Unprovoked - 6 months

89
Q

Treatment of CHADSVASC scores 0, 1, >2?

A

0 - no antithrombotic, or aspirin
1 - aspirin or warfarin/NOAC
>2 - warfarin/NOAC

90
Q

Contraindications for warfarin? SEs?

A

48 hrs post partum, significant bleeding
Haemorrhagic stroke
SE: haemorrhage, nausea, hepatic damage

91
Q

Mechanism of warfarin?

A

Warfarin decreases the body’s ability to form blood clots by blocking the formation of vitamin K–dependent clotting factors. Vitamin K is needed to make clotting factors and prevent bleeding.

92
Q

What are the vitamin K dependent clotting factors?

A

II, VII, IX and X

2 7 9 10

93
Q

Causes of hyperthyroidism? (4)

A 
Graves disease
Thyroiditis
Toxic nodular goitre
Drugs - amiodarone
Postpartum
94
Q

Presentation of hyperthyroidism? (14)

A 
Weight loss
Diarrhoea
Heat intolerance
Irritability
Hyperactivity
Tremor
Palpitations
Atrial fibrillation
Hyperhidrosis
Infertility, ED
Alopecia
Eye signs
Amenorrhoea
Pretibial myxoedema
95
Q

How may hyperthyroidism present in the elderly?(4)

A

Confusion
Dementia
Apathy
Dementia

96
Q

Eye signs in hyperthyroidism? (6)

A 
Lid lag
Lid retraction
Exopthalmos
Proptosis
Double vision
Opthalmoplegia of upward gze
97
Q

Tests for hyperthyroidism? (6)

A 
Low TSH
High T3 and T4
May be anaemia, hypercalcaemic, high ESR
Check thyroid autoantibodies
Isotope scan
Check eyes
98
Q

What is Graves disease?

A

Most common form of hyperthyroidism - may also be hypo

Associated with smoking

99
Q

Pathophysiology of Graves disease?

A

Autoimmune
Antibodies to the TSH receptor are produced, activating thyrotropin receptors causing smooth thyroid enlargement and increased hormone production

100
Q

Features of Graves?

A

Hyperthyroidism
Diffuse goitre +/- thyroid bruit
Eye disease, pretibial myxoedema, oncholysis

101
Q

What is a thyroid storm?

A

Severe hyperthyroid - confusion, agitation, tachycardia, AF, heart failure/CV collapse, coma

102
Q

Causes of thyroid storm? (4)

A

Recent thyroid surgery/radioiodine
Infection
MI
Trauma

103
Q

Management of thyroid storm? (6)

A 
Sedate
Propanolol
Digoxin
Carbimazole
Hydrocortisone
Treat infection
104
Q

Management of hyperthyroidism? (4)

A

Beta blockers propanolol
Carbimazole - most relapse
Radioiodine - most hypothyroid after
Surgery - thyroidectomy if large goitre/refractive

105
Q

Carbimazole mechanism? CI, SEs

A

Stops iodine conversion into usable form, so thyroid hormones not produced
CI: severe blood disorders due to bone marrow suppression
SE: bone marrow suppression, haemolytic anaemia, severe skin reaction

106
Q

Symptoms of hypothyroidism? (11)

A 
Tired/sleepy
Lethargic
Low mood
Cold intolerance
Weight gain
Constipation
Menorrhagia
Hoarse voice
Decreased memory/cognition
Myalgia
Weakness
107
Q

Signs of hypothyroidism? (11)

A 
Bradycardic
Reflexes slow
Ataxia
Dry thin hair/skin
Yawning (drowsy, coma)
Cold
Ascites, oedema, effusions
Round puffy face/obese
Depression
Immobile
Congestive heart failure
108
Q

Investigations for hypothyroidism?

A

TSH high

T4 low

109
Q

Causes of hypothyroidism? (5)

A 
Primary atrophic hypothyroidism
Hashimotos thyroiditis - rarely hyperthyroid first
IODINE DEFICIENCY
Post thyroidectomy/radioiodine
Drugs - carbimazole, amiodarone, lithium
110
Q

Associations of hypothyroidism?

A

Type 1 DM, Addisons
Turners, Downs
Cystic fibrosis

111
Q

Hypothyroid problems in pregnancy? (6)

A 
Eclampsia
Anaemia
Prematurity
LBW
Stillbirth
PPH
112
Q

Management of hypothyroidism?

A 
Levothyroxine lifelong
(if elderly/ill, lower dose)
113
Q

Complication of hypothyroidism? (3)

A

Hypothyroid coma
Heart disease
Dementia

114
Q

What is diabetes mellitus?

A

Common syndrome caused by lack of or decreased effectiveness of endogenous insulin

115
Q

Primary metabolic derangement in diabetes?

A

Hyperglycaemia

116
Q

What is type 1 diabetes?

A

Usually adolescent onset, caused by insulin deficiency from autoimmune destruction of insulin secreting pancreatic beta cells
Cytoplasmic islet cell antibodies (CIA)

117
Q

Cause of type 1 diabetes?

A

HLA D3 and D4 linked
Autoimmune beta cell destruction
Possible - lack of breastfeeding, CMV/coxsackie exposure

118
Q

Presentation of type 1 diabetes?

A 
Polydipsia
Polyuria
Weight loss
Bacterial/fungal infection
Blurred vision
Ketoacidosis
119
Q

Secondary causes of diabetes? (4)

A

Drugs - steroids, anti retrovirals, thiazides
Pancreatitis, pancreatic surgery/trauma
Cushings disease, hyperthyroid, acromegaly
Pregnancy

120
Q

What is LADA?

A

Latent autoimmune diabetes of adults - form of type 1 DM, slower progression and present later in life

121
Q

Pathogenesis of type 2 diabetes?

A

Decreased insulin secretion (beta cell dysfunction) and increased insulin resistance

122
Q

Cause of type 2 diabetes? (5)

A 
Genetics - Asians, 80% concordance in twins (30% in type 1)
Age - although can occur in teens
Obesity
Lack of exercise
Alcohol and calorie excess
123
Q

How does type 2 diabetes present?

A

Asymptomatic

With complications - MI, peripheral neuropathy

124
Q

What is MODY?

A

Maturity onset diabetes of the young - autosomal dominant, affects young people with positive family history

125
Q

How is diabetes diagnosed?

A

Symptoms AND raised venous glucose detected once, or raised glucose on 2 separate occasions
Fasting >/=7mmol/L
Random >/=11.1mmol/L
HbA1c >/=49mmol/L (glycosylated Hb over 3 months)

126
Q

What is metabolic syndrome?

A 
Central obesity and 2 of:
BP >130/85
Triglycerides >1.7mmol/L
HDL <
Fasting glucose >5.6 or DM
127
Q

General advice for diabetes? (4)

A

Lifestyle - exercise, diet, smoking
Statin
Control BP
Foot care

128
Q

Diet recommended in diabetes? (4)

A

Low saturated fats
Low sugar
High starch
Moderate protein

129
Q

Do diabetics need to inform DVLA?

A

Yes

Do not drive if hypoglycaemic spells - loss of doing this may lead to loss of licence

130
Q

Advice for insulin users?

A

Self adjust dose if exercise/ill/increased calories
Avoid binge drinking
Glucogel if needed

131
Q

Main types of SC insulin therapy? (4)

A

Ultrafast acting - novorapid - start of meal or just after
Variable 4-12hr peak - Isophane insulin
Premixed insulin - Novomix - 30% short acting 70% long
Long acting - recombinant human insulin analogues - insulin glargine used at bedtime

132
Q

Common insulin regimens? (3)

A

BD biphasic - twice daily premixed
QDS - ultra fast before meals, bedtime long acting
OD nocte - long acting

133
Q

Methods of insulin delivery?

A

Disposable pens - vary injection site (outer thigh, abdomen) to avoid fatty change
Insulin pump

134
Q

Pharmacological treatment for type 2 diabetes?

A 
Metformin (biguanide)
Gliclazide (sulfonylurea)
Insulin or
Glitazone (thiazolidinediones)
DPP-4 inhibitors (sitagliptin)
SGLT-2 inhibitors (gliflozin)
GLP-1 mimetic (exenatide)
135
Q

How does metformin work? CI, SEs

A

Metformin is a biguanide, increases insulin sensitivity

CI: acute metabolic acidosis inc. DKA, caution in renal damage
SE: GI upset, weight loss

136
Q

How does gliclazide work? CI, SEs

A

Gliclazide is a sulfonylurea, increases insulin secretion

CI: ketoacidosis
SEs: HYPOGLYCAEMIA, weight gain

137
Q

How does glitazone work? CI, SEs

A

Glitazone is a thiazolidinedione, reduces peripheral insulin resistance and lowers blood sugar

CI: congestive heart failure, osteoporosis
SEs: fractures, fluid retention, weight gain

138
Q

How does sitagliptin work? CI, SEs

A

Inhibits dipeptidylpeptidase-4 to increase insulin secretion and lower glucagon secretion

CI: ketoacidosis
SEs: headache, constipation, dizzy

139
Q

How does gliflozin work? CI, SEs

A

Inhibits sodium glucose co-transporter 2 in the kidney so glucose resorption is reduced, urinary glucose exrection increased

CI: ketoacidosis, CV disease - risk of hypotension
SE: constipation, hypotension, HYPOGLYCAEMIA

140
Q

How does exenatide work? CI, SEs

A

Activated glucagon-like peptide 1 receptor to increase insulin secretion, suppress glucagon, and slow gastric emptying

CI: ketoacidosis, severe GI disease
SE: weight loss, GI upset

141
Q

What is diabetic ketoacidosis?

A

Ketoacidosis is an alternative metabolic pathway to carbohydrate metabolism, normally used in starvation states, produces acetone
Occurs in type 1 diabetes as there is excess glucose but lack of insulin so it can’t be utilised, creating starvation state

142
Q

Presentation of DKA? (5)

A 
Gradual drowsiness, coma
Vomiting and dehydration
Abdo pain
Ketotic pear drop breath
Kussmal breathing - deep sighing hyperventilation
143
Q

Triggers of DKA? (6)

A 
Infection
Surgery
MI
Pancreatitis
Drugs - chemo, antipsychotics
Wrong insulin dose/non compliance
144
Q

Diagnosis of DKA?

A

Acidaemia <7.3 blood pH
Hyperglycaemia
Ketonaemia

145
Q

Management of DKA? (6)

A

ABC approach
Bolus saline
Test for pH, bicarb, glucose, ketones, U+Es
Fluids and insulin IV
Reassess blood, possible K+ replacement
Start glucose fluids to prevent hypoglycaemia

146
Q

What is a hyperglycaemic hyperosmolar coma? HONK

A

Hyperglycaemia without ketosis/acidosis

Usually type 2

147
Q

What causes hyperglycaemic hyperosmolar state?

A

Sugary food
Drugs - steroids, thiazides
illness or infection

148
Q

Presentation of hyperglycaemic hyperosmolar state?

A

Dehydration

Danger of occlusive events - focal CNS signs, DIC, leg ischaemia

149
Q

Management of hyperglycaemic hyperosmolar state?

A

Rehydrate
Replace potassium
Small amount of insulin
LMWH prophylaxis

150
Q

What are the major complications of diabetes?

A

Diabetic nephropathy
Diabetic retinopathy
Diabetic neuropathy
Vascular disease

151
Q

How to prevent microvascular complications in diabetes?

A

Good hyperglycaemic control
Treat BP, cholesterol (STATIN)
Stop smoking, exercise, lose weight

152
Q

What is BP target in diabetes?

A

<140/80

153
Q

Most common cause of death in diabetes?

A

Vascular disease - MI (more likely to be silent), stroke

Statin, control BP, aspirin if previous stroke/MI

154
Q

How to reduce risk of vascular event? (3)

A

Statin, control BP, aspirin if previous stroke/MI

155
Q

How to protect the kidneys from nephropathy?

A

ACE inhibitor or ARB - inhibit RAAS and lowers glomerular pressure
Possible spironolactone

156
Q

Mechanism of nephropathy in diabetes? (4)

A

Afferent arteriole more dilated than efferent
High GMR and forces
Cell hypertrophy and thickened basement membrane
Glomerular sclerosis
Causes microalbuminuria

157
Q

What eye problems occur in diabetes? (3)

A

Diabetic retinopathy (background, pre-proliferative, proliferative)
Maculopathy
Cataracts
Rubeosis iridis - new vessels on iris

158
Q

How is diabetic retinopathy managed? (3)

A

Annual screening
Laser photocoagulation - stops angiogenic factors from the ischaemic retina
Possibly give aspirin

159
Q

Mechanism of diabetic retinopathy?

A

Hyperglycaemia and hypertension causes high retinal blood flow
Causes microvascular occlusion, haemorrhages, hypoxia and new vessel formation
New vessels can proliferate, bleed, fibrose and detach the retina

160
Q

How does diabetic retinopathy present?

A

Painless gradual loss o central vision
Cataracts
Floaters

161
Q

What causes diabetic neuropathy?

A

Hyperglycaemia damages Schwann cells

Microvascular damage of nerve blood vessels

162
Q

Types of diabetic neuropathy? (3)

A

Sensory polyneuropathy - glove and stocking paraesthesia
Mononeuritis multiplex - III and VI CNs
Autonomic neuropathy - hypotension

163
Q

Management of neuropathic pain?

A

Amitriptyline
Gabapentin
Pregabalin

164
Q

How does diabetic foot develop? (4)

A

Sensory deficit
Decreased awareness of injury
Motor deficit - distortion of weight
Autonomic deficit - poor control of sweating, vascular supply

165
Q

Typical presentation of diabetic foot?

A 
Painless punched out ulcer
Thick callous
Infection - abscess, cellulitis
Absent ankle jerk
Deformity - pes cavus, claw toes, loss of arch, rocker bottom foot
166
Q

Investigations of diabetic foot? (4)

A

Degree of sensory loss
Ischaemia - foot pulses absent, cold foot, do Doppler pressure measurements
X ray - deformity i.e. Charcot’s joint caused by unimpeded mechanical stress
Infection - swabs, cultures

167
Q

Management of diabetic foot? (4)

A

Regular chiropody
Therapeutic shoes
Abx if infection
Possible surgery - excision and drainage, vascular reconstruction, amputation if deep/rapid spreading infection

168
Q

Serious complications of diabetic foot?

A

Gangrene
Osteomyelitis
Needs amputation

169
Q

How does insulin work?

A

Made in the beta cells in the pancreas islets of Langerhans
Promotes absorption of glucose from the blood into the liver and muscle to be stored as glycogen
GLUCAGON promotes stored glycogen to be turned into glucose and used for energy

3A REVISION (17 decks)

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