Practice Paper 5 Flashcards
What are the 3 types of dementia
ALZHEIMER’S DISEASE (50%) - degeneration of the cerebral cortex, with cortical atrophy and reduction in acetylcholine production
VASCULAR DEMENTIA (25%) - brain damage due to several incidents of cerebrovascular disease (e.g. strokes/TIAs)
LEWY BODY DEMENTIA (15%) - deposition of abnormal proteins (Lewy bodies) within the brain stem and neocortex
PC of alzheimer’s
insidious onset
PC of lewy body dementia
Fluctuating levels of consciousness, hallucinations, falls and Parkinsonian symptoms
Which system in the liver do quinolone AB use?
they inhibit cytochrome p450
Which other drug uses cyt p450 system and hence can’t be sued with quinolones?
warfarin
Define T1DM
Metabolic hyperglycaemia
Caused by absolute insufficiency of pancreatic insulin production
What causes T1DM
autoimmune destruction of b cells (insulin producing cells of the pancreas)
due to genetic susceptibility combined with an environmental trigger
PC of T1DM
Juvenile onstet <30yo Polyuria Polydipsia Nocturia Tiredness Weight loss
Investigations of T1DM
Blood glucose:
- fasting >7
OR
- random >11.1
Hba1c, U&E’s (hyperkalemia prone)
Whats the MX of T1DM
Conservative - advice and pt education
Short acting insulin 3/day before meails
- Lispro, Aspart, Detemir
Long acting insulin 1/day
- Isophane, Glargine, Detemir
Insulin pumps
Monitoring capillary blood glucose levels
Monitoring HbA1C every 3-6months
Screening for complications
Hypoglycaemia mx
If reduced consciousness:
50ml of 50% glucose IV
OR
1mg glucagon IM
If consciousness is normal:
50g oral glucose + starchy meal
What are the complications of T1DM
DKA
Microvascular: retinopathy, neuropathy, nephropathy
Macrovascular: peripheral vascular disease, IHD, Stroke/TIA’s
Increased risk of infections
What are the complications of mx of T1DM
Weight gain
Fat hypertrophy at injection sites
Hypo’s
How do hypoglycemic episodes present
Fits Confusion Coma Tachycardia Palpitations Tremor Hunger Personality changes
What is the prognosis for T1DM
good when early diagnosis, good mx, good glucose control and good compliance
Main causes of morbidity+mortality are vascular disease and renal failure
How does DKA present?
Nausea Vomiting Abdominal pain Polyuria/Polydipsia Drowsiness Confusion Coma Kussmaul breathing Ketotic breath Dehydration
What causes DKA?
Infections
Errors in mx
Newly diagnosed T1DM
Idiopathic
What ix do you need to do for DKA?
WCC (might be raised) U&E's: High urea, High Creatinine *** (due to dehydration) LFT CRP Glucose Amylase ABG - metabolic acidosis with high anion gap Blood&Urinary ketones
What does an ABG show in DKA?
Metabolic acidosis with high anion gap
Whats the mx of DKA? **
50U soluble insulin in 50ml of normal saline
Use insulin sliding scale
Continue with this until: capillary ketone are <0,3, venous pH is above 7.30 and venous HCO3- is above >18mmol
Then change to SC Insulin
(but continue IV for 1-2hrs)
500ml normal saline over 15-30mins until SBP is >100
K+ replacement
Monitori: BG, capillary ketones, urine output = catheterise, U&E’s, VBG.
Broad spectrum AB if there’s infection
Thromboprophylaxis
NBM for atleast 6 hrs
NG tube if GCS is reduced
Define T2DM
Increased peripheral resistance to insulin action, impaired insulin secretion, increased hepatic glucose output
What causes T2DM
Genetic + Environment (MODY)
Obesity
2’ to pancreatic disease, endocrine disease, drugs.
Whats the PC of T2DM pts
Incidental finding sometimes Polyuria Polydipsia Tiredness Infections - Balantis*, Foot ulcers, Candidiasis Hyperosmolar Hyperglycaemic State - HHS
What are the signs OE for T2DM
Increased BMI usually
Increased waist circumference
BP
Diabetic foot: dry skin, loss of SC tissue, ulceration, gangrene, charcot’s arthropathy, weak foot pulses.
SKIN CHANGES (rare): o Necrobiosis lipoidica diabeticorum (well-demarcated plaques on shins or arms with shiny atrophic surface and redMbrown edges)
o Granuloma annulare (flesh-coloured papules coalescing in rings on the back of hands and fingers)
o Diabetic dermopathy (depressed pigmented scars on shins)
What IX do you do for T2DM
1 or more of the following is required to diagnose T2DM:
- Symptomatic patient + random plasma glucose >11.1
- Fasting plasma glucose >7
- 2hr plasma glucose >11.1 after 75g OGTT
What things need to be monitored in T2DM
HbA1C U&E's Lipid profile eGFR Urine albuime: Creatinine ratio
Whats the medication steps in T2DM
At diagnosis: Lifestyle + Metformin (step 1)
If HbA1C >7% after 3 months: step 1 + sulphonylurea
If HbA1C >7% after 3 months: step 1 + basal insulin
If HbA1C >7% after 3 months: add premeal rapid acting insulin
Whats the mx of T2DM
Medicines
Screening for: retinopathy, nephropathy, diabetic foot, vascular disease, CVD - bp, chol.
Pregnant women need strict glycemic control
Whats the mx of HHS
Similar to DKA
+ use 0,45% saline if serum Na+ is >170mmol
- 50 U insuline in 50ml normal saline
- SC insulin
- 500ml normal saline bolus
- Thromboprophylaxis
- K+ replacement
- NBM
What are the complications of T2DM
HHS (due to insulin deficiency, dehydration, raised sodium, raised glucose, raised osmolality, no acidosis though)
Nephropathy: microalbuminuira, proteinuria, renal failure, UTI recurrence.
Retinopathy: background, pre-proliferative, proliferative, more prone to glaucoma and cataracts.
Macrovascular: IHD, stroke, Peripheral vascular disease
What tests do you run on a pre diabetic pt
IFG - impaired fasting blood glucose is 5,6-6,9
IGT - impaired glucose tolerance gives plasma 7.8-11 2hrs after 75mg OGTT.
Whats the triad of cardinal biochemical features for DKA
Hyperglycaemia
Hyperketonaemia
Metabolic Acidosis
Whats the pathophysiology of DKA
The hyperglycaemia causes dehydration and electrolyte loss especially Na+ and K+ through osmotic dieresis.
Ketosis is caused by insulin deficiency and it is exacerbated by elevated catecholamines and other stress hormones resulting in unrestrained lipolysis to free fatty acids for ketogenesis in the liver.
The resulting metabolic acidosis causes the exchange of hydrogen ions for IC K+ although there is also K+ loss through the kidney and intestine.
What are prelevant RF for atherosclerosis?
Smoking LDL cholesterol Hypertension Lack of exercise Obesity (preventable RF)
Secondary causes:
Poor mx of diabetes
Alcohol consumption causes
both cause hypertension
What TFT’s results do you expect normally in a hypothyroidism pt?
Low t4 and high TSH
What are you suspecting if a pt presenting with classic hypothyroidism symptoms has TFT’s of low t4 and low TSH and has bitemporal hemianopia
What test do you want to do?
Suspect central hypothyroidism (2’ hypothyroidism)
Due to a pituitary adenoma
Request an MRI
Define sickle cell disease
A chronic condition with sickling of red blood cells caused by inheritance of haemoglobin S (HbS)
Explain the pathophysiology of sickle cell disease
• Autosomal recessive
• Caused by a point mutation in the beta-globin gene resulting in the substitution of glutamic acid in position 6 by valine
• This results in the formation of abnormal haemoglobin S
• Deoxygenation of HbS alters the conformation resulting in sickling of red cells
• Sickling makes the red cells more fragile and inflexible
• These sickled red cells are prone to:
o Sequestration and destruction (reduced red cell survival ~ 20 days)
o Occlusion of small blood vessels causing hypoxia, which leads to further sickling and occlusion
What factors precipitate sickling
o Infection
o Dehydration
o Hypoxia
o Acidosis
Summarise the epidemiology of sickle cell disease
- Rarely presents before 4-6 months (because HbF can compensate for the defect in adult haemoglobin)
- Common in Africa, Caribbean, MiddleMEast and other areas with a high prevalence of malaria
Recognise the presenting symptoms of sickle cell disease
Symptoms secondary to VASO-OCCLUSION or INFARCTION: o Autosplenectomy (splenic atrophy or infarction) = Leads to increased risk of infections with encapsulated organisms (e.g. pneumococcus, meningococcus)
o Abdominal Pain
o Bones
• Painful crises affect small bones of the hands and feet causing dactylitis in CHILDREN
• Painful crises mainly affect the ribs, spine,
pelvis and long bones in ADULTS
o Myalgia and Arthralgia
o CNS
• Fits and strokes
o Retina
• Visual loss (proliferative retinopathy)
Symptoms of SEQUESTRATION CRISIS
o NOTE: sequestration crises occur due to pooling of red cells in various organs (mainly the spleen)
o Liver –> exacerbation of anaemia
o Lungs --> acute chest syndrome • Breathlessness • Cough • Pain • Fever
o Corpora cavernosa
• Persistent painful erection (priapism)
• Impotence
Recognise the signs of sickle cell disease on physical examination
Signs secondary to VASO-OCCLUSION, ISCHAEMIA or INFARCTION
o Bone - joint or muscle tenderness or swelling (due to avascular necrosis)
o Short digits - due to infarction in small bones of the hands
• Retina - cotton wool spots due to retinal ischaemia
• Signs secondary to SEQUESTRATION CRISES
o Organomegaly
• The spleen is ENLARGED in early disease
• Later on, the spleen will reduce in size due to splenic atrophy
o Priapism
• Signs of anaemia
Identify appropriate investigations for sickle cell disease
BLOODS: o FBC • Low Hb * • Reticulocytes: - HIGH - in haemolytic crises - LOW - in aplastic crises o U&Es
• Blood Film o Sickle cells o Anisocytosis (variation in size of red cells) o Features of Hyposplenism: • Target cells • Howell-Jolly bodies
• Sickle Solubility Test
o Dithionate is added to the blood
o In sickle cell disease you get increased turbidity *
• Haemoglobin Electrophoresis
o Shows HbS
o Absence of HbA (if homozygous HbS)
o High HbF
• Hip X-Ray
o Femoral head is a common site of avascular necrosis *
• MRI or CT Head
o If there are neurological complications
What do you expect a blood film of a sickle cell disease pt to look like
o Sickle cells o Anisocytosis (variation in size of red cells) o Features of Hyposplenism: • Target cells • Howell-Jolly bodies
Generate a management plan for sickle cell disease
• Infection Prophylaxis
o Penicillin V
o Regular vaccinations (particularly against capsulated bacteria e.g. pneumococcus)
• Folic Acid
o If severe haemolysis or in pregnancy
• Hydroxyurea/Hydroxycarbamide *
o Increases HbF levels
o Reduces the frequency and duration of sickle cell crisis
• Red Cell Transfusion
o For SEVERE anaemia
o Repeated transfusions (with iron chelators) may be required in patients suffering from repeated crises
• Advice
o Avoid precipitating factors, good hygiene and nutrition, genetic counselling, prenatal screening
• Surgical
o Bone marrow transplantation
o Joint replacement in cases with avascular necrosis
Whats the mx for acute painful crisis of sickle cell disease
• ACUTE (PAINFUL CRISES) o Oxygen o IV Fluids o Strong analgesia (IV opiates) o Antibiotics
Identify the possible complications of sickle cell disease
- Aplastic crises
- Haemolytic crises
- Pigment gallstones
- Cholecystitis
- Renal papillary necrosis
- Leg ulcers
- Cardiomyopathy
Whats an aplastic crisis
• Aplastic crises
o Infection with Parvovirus B19 can lead to a temporary cessation of erythropoiesis (which can cause red cell count to plummet in sickle cell patients because their red cells have a shortened life span and can’t tolerate a cessation of erythropoiesis)
Summarise the prognosis for patients with sickle cell disease
• Most patients with sickle cell disease who manage their disease well will survive until around the age of 50 yrs
• Mortality is usually the result of:
o Pulmonary or neurological complications in ADULTS
o Infection in CHILDREN
What are the symptoms of sedative withdraw?
Nausea Vomiting Autonomic hyperactivity Insomnia Delirium Seizures
Known coeliac disease pt comes in with itchy rash on both forearms with evidence of blistering
What is it
Dermatitis Herpetiformis
• Intense, itchy blisters on elbows, knees or buttocks
What are the cutaneous features of Crohn’s?
Perianal abscess
Fistulae
Skin tags
Apthous ulcers
What are the cutaneous features of UC?
Erythema nodosum
Pyoderma gangrenosum
What are the cutaneous features of Sarcoidosis?
Erythema nodosum Lupus pernio (purple indurated lesions)
Identify the possible complications of Crohn’s disease
• GI: o Haemorrhage o Strictures o Perforation o Fistulae (between bowel, bladder, vagina) o Perianal fistulae and abscesses o GI cancer o Malabsorption
• Extraintestinal Features: o Uveitis o Episcleritis o Gallstones o Kidney stones o Arthropathy o Sacroiliitis o Ankylosing spondylitis o Erythema nodosum o Pyoderma gangrenosum o Amyloidosis
What is the chronic mx of crohn’s?
Long-Term
o Steroids - for acute exacerbations
o 5-ASA analogues - decreases the frequency of relapses (useful for mild to moderate disease)
• NOTE: more commonly used in UC
o Immunosuppression: using steroid-sparing agents (e.g. azathioprine, 6-mercaptopurine, methotrexate) reduces the frequency of relapses
o Anti-TNF agents: (e.g. infliximab and adalimumab) - very effective at inducing and maintaining remission. Usually reserved for refractory Crohn’s.
• General Advice:
o Stop smoking
o Dietician referral (low fibre diet necessary if there are stricture present)
• Surgery indicated it:
o Medical treatment fails
o Failure to thrive in children in the presence of complications
o Involves resection of affected bowel and stoma formation M NOTE: there is a risk
of disease recurrence
Recognise the presenting symptoms of ulcerative colitis
- Bloody or mucous diarrhoea (stool frequency depends on severity of disease)
- Tenesmus and urgency
- Crampy abdominal pain before passing stool
- Weight loss
- Fever
- Extra-GI manifestations (e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum)
Recognise the presenting symptoms of Crohn’s disease
- Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)
- Diarrhoea (may be bloody or steatorrhoea)
- Fever, malaise, weight loss
- Symptoms of complications
- Sometimes right iliac fossa pain* due to inflammation of terminal ileum
Why should you not administer high flow o2 in type 2 respiratory failure with respiratory acidosis?
It will lead to worsening of the hypercapnic respiratory failure
What is chronic bronchitis
Chronic cough and sputum production on most days for at least 3 months per year over 2 consecutive years
Narrowing of the airways resulting in bronchiole inflammation (bronchiolitis) Bronchial mucosal oedema Mucous hypersecretion Squamous metaplasia
What is emphysema
Pathological diagnosis of permanent destructive enlargement of air spaces distal to the terminal bronchioles
Destruction and enlargement of alveoli
Leads to loss of elasticity that keeps small airways open in expiration
Progressively larger spaces develop called bullae (diameter > 1 cm)
Recognise the presenting symptoms of COPD
Chronic cough Sputum production Breathlessness Wheeze Reduced exercise tolerance
Recognise the signs of COPD on physical examination
INSPECTION Respiratory distress Use of accessory muscles Barrel-shaped over-inflated chest Decreased cricosternal distance Cyanosis
PERCUSSION Hyper-resonant chest Loss of liver and cardiac dullness Auscultation Quiet breath sounds Prolonged expiration Wheeze Rhonchi - rattling, continuous and low-pitched breath sounds that sounds a bit like snoring. They are often caused by secretions in larger airways or obstructions Sometimes crepitations
SIGNS OF O2 RETENTION
Bounding pulse
Warm peripheries
Asterixis
LATE STAGES: signs of right heart failure (cor pulmonale)
Right ventricular heave
Raised JVP
Ankle oedema
What might you expect in the FBC of a COPD pt
Increased Hb and haematocrit due to secondary polycythaemia
