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Medicine Finals > finals > Flashcards

finals Flashcards

0
Q

Huntingtons - chromosome, repeat, pathology

A

Chromosome 4 - cag repeat - huntingtin protein

Decreased GABA neurons in basal ganglia leads to increases stimulation of thalamus and cortex by global pallidus

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1
Q

Alzheimer’s - pathology

A

Beta amyloid plaques
Neurofibrillary tangles - tau proteins
Cerebral atrophy, peri ventricular degeneration
Affects posterior parietal lobe

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2
Q

Alzheimer’s drug treatment?

A

If mmse >12 - acetylcholinesterase inhibitors - donepezil, rivastigmine, galantamine
<12 - nmda receptor antagonist - memantine

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3
Q

Lewy body dementia - pathology, treatment

A 
Lewy bodies (eosinophilic aggregates, ubiguitin) - widespread in subcortical areas and temporal cortex
No treatment - avoid antipsychotics as they may be neuroleptic sensitive - get very bad epse's
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4
Q

Frontotemporal dementia - picks disease - pathology

A

Frontotemporal atrophy, knife blade atrophy, picks bodies (contain tau)

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5
Q

Neurosyphilis

A

General paresis - dementia, frontal lobe dysfunction, ar pupils
Tabes dorsalis - shooting pains, ataxia

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6
Q

Alcohol dependence

A 
Primacy
Compulsion to drink
Narrowing of repertoire
Increased tolerance
Withdrawal symptoms 
Continuing drinking to avoid withdrawal
Reinstatement after abstinence
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7
Q

Delirium tremens

A

72 hrs after last drink
Tachycardia hypertension, tremor, fits, visual tactile hallucinations, worse at night
Rx: bdz reducing regime (chlordiazepoxide), thiamine b1

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8
Q

Maintenance of alcohol detox

A

Disulfiram - Antabuse - acetaldehyde
Acamprosate - reduces cravings by enhancing GABA
Naltrexone - partial opioid receptor antagonist - reduces cravings

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9
Q

Wernickes encephalopathy

A

B1 deficiency causes mammillary body damage

Nystagmus
Ataxia
Peripheral neuropathy
Clouding of consciousness
Ophthalmoplegia

Rx - pabrinex

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10
Q

Korsakoffs psychosis

A

Anterograde amnesia
Retrograde amnesia
Preservation of immediate recall
Confabulation

Irreversible

Give oral thiamine

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11
Q

Opioid dependence - treatment

A

Methadone
Buprenorphine - partial opioid receptor antagonist - start when not using very much meth
Naltrexone - opioid receptor antagonist - use after stopped to prevent relapse

Naloxone - for overdoses

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12
Q

Benzodiazepines - how do they work

A

Enhance GABA activity

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13
Q

Cocaine - neurotransmitters involved?

A

Dopamine, serotonin, noradrenaline - blocks reuptake

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14
Q

Test for cystic fibrosis

A

Immunoreactive trypsinogen

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15
Q

ECG changes in PE?

A

Rv hypertrophy
Sinus tachycardia
S1Q3T3

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16
Q

ECG changes in left atrial hypertrophy?

A

P mitrale - broad bifid p waves - due to mitral stenosis

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17
Q

ECG changes in right atrial hypertrophy?

A

P Pulmonale - peaked p wave - tricuspid stenosis or pulmonary hypertension

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18
Q

What type of drug is a statin?

A

Hmg coa reductase inhibitor

Sfx - muscle pain, rhabdomyolosis, elevated lfts

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19
Q

What is cushings disease?

A

ACTH excess causing high cortisol levels

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20
Q

Hormonal treatment for acromegaly?

A

Octreotide - a somatostatin analogue

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21
Q

What is kallmans syndrome?

A

Failure of gnrh secretion - 50% have loss of smell

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22
Q

What is Hashimoto’s thyroiditis?

What are the antibodies?

A

Atrophic changes with regeneration leading to goitre formation
Thyroid peroxidase antibodies

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24
Q

Graves’ disease antibodies and special features?

A

Tsh receptor antibodies

Specific eye signs - Ophthalmoplegia and exophthalmos

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25
Q

What is extramedullary haematopoeisis and when does it occur?

A

Haematopoesis that starts occurring in liver and spleen and places other than marrow - occurs in states where marrow has been replaced eg myelofibrosis, myeloproliferative disorders, and in excessive demand eg haemoglobinopathies

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26
Q

What cells are produced from common myeloid progenitors?

A

Megakaryocytes, erythrocytes, mast cells, basophils, neutrophils, eosinophils, monocytes

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27
Q

What cells are produced from common lymphoid progenitors?

A

natural killer cells, t lymphocytes, b lymphocytes

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28
Q

Where do lymphocytes mature?

A

Thymus

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29
Q

Which white blood cells are granulocytes

A

basophils, eosinophils, neutrophils, nk cells

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30
Q

Role of neutrophils

A 
Engulf & kill bacteria
Release cytokines (IL1, TNFalpha) and chemotaxins (adhesion molecules)
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31
Q

Role of eosinophils

A

Similar function to neutrophils
Act against parasites
Involved in hypersensitivity

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32
Q

Role of monocytes

A

Migrate to tissues and become either dendritic cells (present antigens) or macrophages (engulf pathogen and present antigens)

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33
Q

Role of basophils & mast cells

A

Mediate parasite and allergic reactions, like eosinophils
Have surface receptors for IgE
Release heparin and histamine

Mast cells = v similar but stay on connective tissue not blood

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34
Q

Role of T lymphocytes

A

CD4 helper cells - bind to MHCs on antigen presenting cells and produce cytokines which activate B cells and macrophages
CD8 cytotoxic cells - bind to MHCs on antigen presenting cells and kill cells infected by pathogens

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35
Q

Role of natural killer cells

A

Destroy native cells which are abnormal or infected by pathogens - part of innate response - important in the bodys response to cancer

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36
Q

Role of B lymphocytes

A

When activated by T helper cells, some become plasma cells and produce antibodies, some become memory cells which stay around after the infection and have v sensitive immunoglobulins which will detect and respond to low levels of the same pathogen in the future

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37
Q

Roles of the spleen

A

Phagocytosis of old RBCs
Pools WBC and platelets, can be rapidly mobilised when needed
Some first-line immunological defence
Extramedullary haematopoesis

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38
Q

Causes of massive splenomegaly

A 
CML
Myelofibrosis
Chronic malaria
Leishmaniasis
Gauchers (lysosomal storage disease --> lipid accumulation)
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39
Q

Complications of splenectomy

A

Infection - vaccinations & lifelong oral Pen V
Thromobocytosis for 2-3 wks afer
Abnormal RBC morphology - Howell-Joly bodiesm Pappenheimer bodies, target cells etc

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40
Q

Causes of splenic atrophy

A

Sickle cell disease (infarctions)

Coeliac disease

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41
Q

Causes of microcytic anaemia

A

Iron deficiency
Thalassaemia
Sideroblastic anaemia
Anaemia of chronic disease

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42
Q

Causes of macrocytic anaemia

A

Megaloblastic - B12 and folate def

Normoblastic - liver disease, hypoTH, alcohol, drugs, aplastic anaemia, pregnancy, myeloma

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43
Q

Causes of normocytic anaemia

A

Haemorrhage, haemolysis, anaemia of chronic disease

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44
Q

What is sideroblastic anaemia?

A

Consider if microcytic anaemia does not respond to Fe
DIsorder of haem synthesis resulting in refractive anaemia, microcytics hypochromic RBCs, ring sideroblasts in BM
May be due to myelodysplasia, alcohol, isoniazid

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45
Q

Causes of red cell aplasia

A

Diamond blackfan
Transient erythroblastopenia of childhood (post viral)
Parvovirus B19

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46
Q

Causes of aplastic anaemia

A 
Fanconis anaemia (AR)
Idiopathic
Cytotoxic drugs
Radiation
Infection
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47
Q

Investigations for Fe def anaemia

A 
Low Hb, low MCV, low MCHC
Low ferritin
Low Fe
High total iron binding capacity (as liver produces more transferrin)
Endoscopy - in older people
Coeliac serology
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48
Q

Drugs which may cause folate deficiency?

A

Trimethoprim, methotrexate, phenytoin, sulfasalazine

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49
Q

Causes of haemolytic anaemia

A

Inherited RBC abnormalities - spherocytosis, G6PD def, thalassaemia, sickle cell
Immune - newborn, blood transfusions
Autoimmune - warm & cold
Mechanical - DIC, HUS, heart valves, marching

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50
Q

Inheritance and pathophysiology of hereditary spherocytosis

A

AD

Mutation of RBC membrane protein eg spectrin - increased permeability to Na - spheroidal shape- destroyed in spleen

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51
Q

Differential diagnosis of spherocytosis

A

Hereditary spherocytosis

Autoimmune haemolytic anaemia - direct Coombes test +ve

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52
Q

Inheritance and pathophysiology of G6PD deficiency

A

X-linked
G6PD is enzyme which maintains glutathione levels and prevents oxidative damage to RBCs - without it, oxidant-induced haemolysis occurs

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53
Q

Warm haemolytic anaemia - antibody type and causes

A

IgG

SLE, lymphoma, CLL, carcinomas, drugs

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54
Q

Cold haemolytic anaemia - antibody type and causes

A

IGM

Infection, paroxysmal cold haemolysis

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55
Q

Triggers for haemolysis in G6PD deficiency

A

Infection, fava beans, quinine, ciprofloxacin, nitrofurantion, sulphonylureas

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56
Q

Sickle cell disease pathology

A 
Mutation in gene for Beta-globin chain --> HbS gene - valine instead of glutamine
If homozygous (HbSS) - nearly all Hb is HbS, which polymerises in low oxygen states, making RBCs sickle shaped and rigid and fragile
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57
Q

4 crises in sickle cell disease

A

-Vasocclusive - painful - dactylitis, pain, avascular necrosis, priapism, stroke
-Sequestration - spleen engorged
-Aplastic - due to Parvovirus
-Haemolytic (rare)
Also increased risk of infection & sepsis

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58
Q

Management of sickle cell crisis

A

analgesia (opioids), hydration, abx if infection, exchange transfusion if severe

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59
Q

Drug used to reduce rate of crises in sickle cell

A

Hydroxyurea/hydroxycarbamide - increased concentration of foetal Hb

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60
Q

B thalassaemia pathophysiology

A

Imbalance of production of alpha and beta chains - beta chain production decreased so cant make HbA - make more HbF and HbA2 instead
Major form - severe anaemia, need regular transfusions + iron chelation (desferrioxamide)

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61
Q

A thalassaemia pathophysiology

A

Problem with genes for alpha globin - fewer normal a globin genes means more b globin chains
Most severe is major (all 4 deleted) -fatal
3 deleted - mild anaemia
1/2 deleted - asymptomatic

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62
Q

Haemophilia - what is deficient in each type?

A

A - factor VIII

B - factor IX

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63
Q

Clotting function test results in haemophilia and VW disease

A

Haemophilia - prolonged APTT
VW - prolonged APTT, prolonged bleeding time (as platelet function abnormal as well as decreased factor VIII)
Both have normal prothrombin time

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64
Q

Treatment of haemophilia and VW disease

A

Replace deficient factor

Desmopressin

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65
Q

Polycythaemia rubra vera pathophysiology

A

Excess proliferation of RBC ± platelets and other cells

95% due to JAK2 mutation –> activates tyrosine kinase

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66
Q

Treatment of polycythaemia rubra vera

A

venesection
chemo - hydroxycarbamide & busulfan to decrease plt count
low dose aspirin
allopurinol

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67
Q

WHO definition of osteporosis

A

BMD at least 2.5 standard deviations below the mean (between -1 and -2.5 is osteopenia)

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68
Q

Risks associated with oestrogen

A 
Breast cancer
Endometrial cancer (if unopposed)
Venous thromboembolic disease
Stroke
Vaginal bleeding
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69
Q

What is raloxifene?

A

Selective oestrogen receptor modulator - acts on oestrogen receptors in bone to increased BMD, but does not affect receptors in endometrium and breast - which is good!!
Sfx - increases menopausal symptoms, increased risk of VTE

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70
Q

What is denosumab?

A

Fully human monoclonal antibody to RANKL - for osteoporosis

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71
Q

What is strontium ranelate?

A

dual action bone agent for osteoporosis - increases bone formation AND decreases bone resorption

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72
Q

Risk factors for osteomalacia

A

Lack of sunshine, dark skin, anticonvulsants, malabsorption, CKD

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73
Q

RA + splenomegaly = ?

A

Feltys syndrome

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74
Q

Extra-articular features of Ank spond?

A

Anterior uveitis
Aortitis/aortic regurg
Apical lung fibrosis
Amyloidosis

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75
Q

Which crystals are present in gout and pseudogout?

A

Gout - monosodium urate - negatively birefringent

Pseudogout - calcium pyrosphosphate - positively birefringent

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76
Q

Side effects of corticosteroids

A 
Weight gain
Osteoporosis
Think skin, bruising, poor wound healing
Hypertension/oedema
Infection
Hyperglycaemia
Psychosis
Cataracts
Muscle weakness/myopathy
Adrenal/pituitary suppression
Pancreatitis
Impaired growth
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77
Q

What is rituximab?

A

Anti-CD20 antibody - causes lysis of B cells

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78
Q

What are the anti TNF drugs?

A

Infliximab - monoclonal antibody against TNF
Etanercept - TNF receptor fusion protein
Adalimumab - monoclonal antibody against TNF

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79
Q

What are complications of blood transfusion? Early & late

A

Early - ABO incompatibility, fluid overload, febrile reaction, urticarial reaction, transmission of infection

Late - RhD and other sensitisation, delayed transfusion reaction, Iron overload, transmission of infection

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80
Q

Causes of red eye

A

Conjunctivitis, keratitis, scleritis, episcleritis, uveitis, acute glaucoma, endophthalmitism subconjunctival haemorrhage

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81
Q

What is the 4th generation test for HIV?

A

ELISA or western blot for HIV antibodies

Test for p24 antigen

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82
Q

Treatment of urge incontinence

A

Anticholinergics - oxybutynin, tolterodine
Sacral neuromodulation
Intravesical botox
Surgery - detrusor myomectomy, cystoplasty
Physiotherapy
Behavioural therapy

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83
Q

Treatment of stress incontinence

A

Pelvic floor exercises, vaginal cones
Weight loss
Surgery - TVT, TOT
Duloxetine (SNRI)

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84
Q

What are the most common types of testicular tumour?

A

90% are germ cell tumours

  • seminomas 48%
  • non-seminomatous 42% - teratoma, yolk sac, choriocarcinoma
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85
Q

What are the tumour markers for testicular ca?

A

beta hcg, afp, palp (placental ALP), LDH

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86
Q

Which drug can reverse the effects of benzos?

A

Flumazenil (benzodiazepine antagonist)

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87
Q

What are the beta lactam abx?

A

Penicillins, cephalosporins and carbapenems
They inhibit cell wall synthesis
Bacteriocidal

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88
Q

What are the aminoglycoside antibiotics?

A

Gentamycin, streptamycin, neomycin
They inhibit protein synthesis
Bacteriocidal

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89
Q

What are the macrolide antibiotics?

A

clarithromycin, azithromycin, erythromycin,
They inhibit translocation of proteins
Bacteriocidal/static

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90
Q

What are the tetracycline antibiotics?

A

Doxycyline, oxytetracycline
Inhibits protein synthesis
Bacteriostatic

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91
Q

What is trimethoprim?

A

A folic acid inhibitor

Bacteriostatic

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92
Q

What is the innervation to the pupil?

A

Afferent - CN2 (optic nerve) - chiasm –> optic tracts –> synapses in lateral geniculate nucleus –> optic radiations –> occipital cortex
Efferent
-Parasympathetic - with CN3 (oculomotor) - arises from Edinger-Westphal nucleus
-Sympathetic - from cervical spinal cord

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93
Q

Causes of miotic pupil

A 
Old age
Opiates
Pilocarpine
Horner's
Pontine lesion
Argyll Robertson pupil (neurosyphilis)
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94
Q

Causes of mydriatic pupil

A

Arousal
Damage to eye eg acute glaucoma, trauma, iritis
Anticholinergics - atropine, oxybutynin, antidepressants
Sympathetic stimulants - cocaine
3rd nerve palsy - eg DM
Midbrain lesion
Holmes Adie pupil

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95
Q

What is Bell’s palsy?

A

Dysfunction of CN7 (facial nerve) –> unilateral facial weakness
(LMN so does NOT spare forehead like a UMN problem would)

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96
Q

What is mild non-proliferative diabetic retinopathy?

A

At least 1 microaneurysm

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97
Q

What is moderate non-proliferative diabetic retinopathy?

A

Microaneurysms or dot/blot haemorrhages ± cotton wool spots, venous beading, IRMAs, hard exudates

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98
Q

What is severe non-proliferative diabetic retinopathy?

A

Blot haems + microaneurysms in 4 quadrants
Venous beading in at least 2 quadrants
IRMA in at least 1 quadrant

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99
Q

What is proliferative diabetic retinopathy?

A 
Retinal neovascularisation (may cause vitreous haem)
Fibrous tissue forms anterior to retinal disc
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100
Q

What is maculopathy?

A

Any background changes, haemorrhage, oedema or ischaemia of the macula –> may affect vision

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101
Q

Management of diabetic retinopathy

A

Glycaemic & risk factor control
Focal or panretinal photocoagulation
Anti-VEGF - Pegaptanib, bevacizumab and ranibizumab
Intravitreal steroids

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102
Q

Hypertensive retinopathy - grades

A

1 - barely detectable arterial narrowing (silver wiring)
2 - arterial narrowing & focal irregularities (AV nipping)
3 - + flame haemorrhages, exudates, cotton wool spots
4 - + disc swelling

May also get Elschnig spots & Siegrist streaks

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103
Q

Management of glaucoma

A

Decrease secretion - topical beta blockers, topical/PO carbonic anhydrase inhibitors (acetazolamide)
Increase outflow - topical prostanoids, topical alpha agonists
Laser - trabeculoplasty, iridotomy
Surgical - trabeculectomy

If acute closed angle - IV acetazolamide, beta blockers, pilocarpine (parasympathomimetic, constrict pupil to open angle), iridotomy

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104
Q

Prevention of thyroid eye disease in Grave’s?

A

Stop smoking!

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105
Q

What are the symptoms and signs of chronic open angle glaucoma?

A

May be no visual changes
May get loss of peripheral fields, starting nasally, ending up with tunnel vision
O/e - optic disc cupping with notched rim
With gonioscopy lens - open angle visible at iridocorneal angle

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106
Q

What are the symptoms and signs of acute closed angle glaucoma?

A 
Sudden onset severe eye pain - worse with mydriasis
Blurred vision
Watering
Photophobia
Visual haloes
N, V, abdo pain
Fixed semidilated pupil
Cloudy cornea
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107
Q

SIgns and symptoms of retinal artery occlusion

A

Sudden painless visual loss

PALE retina, cherry red spot at fovea

108
Q

Signs and symptoms of retinal vein occlusion

A

Sudden painless loss of vision

Severe haemorhages, tortuous dilated retinal veins, macular oedema, cotton wool spots - cheese and tomato pizza!

109
Q

Causes of anterior ischaemic optic neuropathy

A

Arteritis - eg temporal!

Atherosclerosis

110
Q

How to manage a pregnant woman exposed to chicken pox?

A 
If >20wks gestation - v low risk of transmission
If <20wks...
-Check antibodies
-If not immune, give VZ immunoglobulin
-If rask present, give aciclovir
111
Q

Classification of hypertension in pregnancy

A

Pre-existing hypertension = 140/90 before 20 wks
Pregnancy-induced hypertension = 140/90 after 20 wks, no proteinuria
Pre-eclampsia = 140/90 after 20 wks + proteinuria >0.3g/24hrs

112
Q

What is Meig’s syndrome?

A

Benign ovarian tumour (normally fibroma) + ascites + pleural effusion

113
Q

Most common benign ovarian tumour in young women

A

Dermoid cyst (teratoma)

114
Q

Most common cause of ovarian enlargement in women of reproductive age

A

Follicular cyst

115
Q

Which HPVs are associated with cervical ca?

A

16,18, 33

6 and 11 are warts

116
Q

Risks associated with HRT?

A

Increased risk of breast ca, endometrial ca (reduced by adding progestogen), VTE, stroke, ischaemic heart disease

117
Q

What is Fitz Hugh Curtis syndrome?

A

RUQ pain and perihepatitis caused by PID

118
Q

Treatment of chlamydia?

A

Single dose azithromycin or 7 days doxycycline

119
Q

Benefits of HRT?

A

Alleviates vasomotor symptoms (flushing, headaches etc)
Prevents osteoporosis
Reduces risk of colorectal ca

120
Q

Why can you get symptoms of thyrotoxicosis with hydatiform moles?

A

Because the high levels of hCG can mimic TSH

121
Q

What disease does Coxsackie A16 virus cause in children?

A

Hand foot and mouth disease = sore throat, fever, vesicles in mouth and on palms and soles

122
Q

What is Scarlet fever?

A

Reaction to erythrogenic toxins produced by Group A haemolytic streptococci
Fever, malaise, tonsillitis
‘Strawberry’ tongue
Rash - fine punctate erythema sparing face
Rx - Pen v

123
Q

How does Rubella infection in a chid present?

A

Rash: pink maculopapular, initially on face before spreading to whole body, usually fades by the 3-5 day
Lymphadenopathy: suboccipital and postauricular

124
Q

What is seborrhoeic dermatitis?

A

Common benign greasy scaling rash caused by yeast (Malassezia sp) - may cause cradle cap in infants

125
Q

Combined test for Downs?

A

Beta hcg + PAPPA + nuchal translucency - at 11-14 weeks

126
Q

Consequences of congenital rubella

A

Sensorineural deafness
Congenital cataracts
Congenital heart disease (e.g. patent ductus arteriosus)
Glaucoma

127
Q

Consequences of congenital toxoplasmosis

A

Cerebral calcification
Chorioretinitis
Hydrocephalus

128
Q

Consequences of congenital CMV

A

Growth retardation

Purpuric skin lesions

129
Q

Treatment of threadworm (pinworm)?

A

Mebendazole & hygiene measures for child & all family

130
Q

What are muscle fibres made up of?

A

Many myofibrils - which have thick myosin and thin actin filaments - actin filaments have troponin and tropomyosin attached for linking to cross bridges on myosin

131
Q

What receptors monitor how much a muscle fibre is being stretched?

A

Muscle-spindle stretch receptors - wrapped round intrafusal muscle fibres

132
Q

Which receptors monitor how much tension a muscle is under?

A

Golgi tendon organs

133
Q

Pathophysiology of Parkinsons

A

Degeneration of substantia nigra in brainstem –> less dopamine released in basal ganglia –> motor cortex activated less

134
Q

Drugs for Parkinsons?

A

Dopamine agonists - ropinirole
Monoamine oxidase B (enzyme breaks down Da) inhibitors - selegeline
Dopamine precursors - Levodopa + peripheral decarboxylase inhibitor

135
Q

What are the amine hormones?

A

Thyroid hormones, catecholamines and dopamine

136
Q

What are the steroid hormones?

A

Cortisol, aldosterone, testosterone, estradiol, 1,25-dihydroxyvitamin D

137
Q

What are the majority of hormones?

A

Peptides

138
Q

What hormones are secreted by each part of the adrenal glands?

A

Cortex
ZG - aldosterone
ZF/ZR - DHEA, androstenedione, cortisol
Medulla - adrenaline, noradrenaline

139
Q

Enzyme necessary for producing thyroid hormones from iodine and thyroglobulin

A 
Thyroid peroxidase (TPO) 
nb anti-TPO antibodies are present in Hashimotos thyroiditis
140
Q

Actions of thyroid hormone

A

Increased basal metabolic rate
Regulate bone growth and neural maturation
Increase bodys sensitivity to catecholamines
Increase body temperature
Fat mobilisation & breakdown
Carbohydrate metabolism
Growth & development in children
Increase heart rat, contractility and cardiac output
Allow normal fertility

141
Q

What is Addisons?

A

Primary adrenal insufficiency

142
Q

What is Conns?

A

Aldosterone producing adenoma

143
Q

What is Cushings disease?

A

Cushings syndrome due to ACTH-secreting tumour of pituitary gland

144
Q

Major effects of growth hormone?

A

Induces secretion of IGF-1 from liver, chondrocytes and other tissues. IGF-1 –> cell division
Stimulate protein synthesis, esp in muscle
Anti-insulin effects

145
Q

Which hormones favour bone formation and which favour resorption?

A

Bone formation: insulin, GH, IGF-1, oestrogen, testosterone, calcitonin
Bone resorption: PTH, cortisol, thyroid hormones

146
Q

What is released in hypercalcaemia of malignancy?

A

PTH-related peptide

147
Q

What is the cause of secondary hyperparathyroidism?

A

Failure to absorb Vit D in gut or decreased 1,25dihydroxyvitamin D production –> increased PTH –> restores calcium levels but at expense of bone

148
Q

What is the cause of pseudohypoparathyroidism?

A

End-organ resistance to PTH (PTH levels are high but ineffective)

149
Q

What is atrial natriuretic peptide?

A

A peptide hormone and powerful vasodilator secreted in the atria in response to high blood volume
Increases GFR, decreases sodium reabsorption, inhibits renin, inhibits aldosterone, vasodilates, increases release of free fatty acids from adipose tissue

150
Q

What is Cushing’s phenomenon?

A

Traumatic head injury leads to increased intracranial pressure, decreased brain blood flow, and a large increase in arterial blood pressure
(because the pressure exerts force on blood vessels so slow is reduced and metabolites build up in brain interstitial fluid causing powerful stimulation of sympathetic neurons controlling systemic arterioles

151
Q

Typical causes of AF

A 
Thyrotoxicosis
Mitral stenosis
Ischaemic heart disease
Pulmonary embolism
Pneumonia
Sepsis
Alcohol 
Cardiomyopathy and other structural / valvular heart diseases.
152
Q

Which hormones are lipid soluble and where are their receptors?

A

Steroids, thyroid hormones and 1,25-dihydroxy Vit D
Bind to intracellular receptor proteins - in nucleus or in cytosol - these receptors act as transcription factors or suppressors

153
Q

Which hormones are water soluble and where are their receptors?

A

Most hormones, neurotransmitters, paracrine/autocrine messengers (apart from Steroids, thyroid hormones and 1,25-dihydroxy Vit D)
Bind to proteins on extracellular surface of plasma membrane - these may be ligand gated ion channels, enzymes or G-protein-coupled receptors - may activate second messengers inside cell

154
Q

How do steroids work?

A

Inhibit phospholipase A2 - which inhibits the formation of arachidonic acid (the origin of prostaglandins, prostacyclin, thromboxane and leukotrienes)
In contrast, NSAIDs inhibit COX, and so inhibit formation of prostaglandins, prostacyclin and thromboxane only

155
Q

Which cells produce the myelin sheath of nerves?

A

CNS - oligodendrocytes

PNS - Schwann cells

156
Q

What produces CSF?

A

Ependymal cells of choroid plexus lining ventricles

157
Q

Where does CSF go in the brain?

A

Subarachnoid space (between arachnoid and pia mater)

158
Q

Where is CSF absorbed?

A

Arachnoid granulation & lymphatic channels

159
Q

What controls the shape of the lens in the eye?

A

The ciliary muscles, and the tension they apply to the zonular fibres
Parasympathetic control

160
Q

What is presbyopia?

A

Lens loses elasticity with age - less able to accommodate for near vision

161
Q

What are the muscles which protect the inner ear from very loud sounds?

A

Tensor tympani (attaches to malleus and TM) and stapedius (attaches to stapes) - contract reflexively to dampen movements of middle ear bones and transmit less sound to inner ear

162
Q

What is the uvea?

A

Choroid, ciliary muscles and iris

163
Q

What neural pathway is involved in rewards and motivation?

A

Mesolimbic dopamine pathway

164
Q

Alzheimers drug rx?

A

Mild-mod: acetylcholinesterase inhibitors - donepezil, rivastigmine, galantamine
Mod-sev: NMDA receptor antagonist - memantine

165
Q

Causes of long QT

A 
Hypocalcaemia, hypokalaemia, hypomagnesaemia
MI/ischaemia
Myocarditis
Hypothermia
Amiodarone, sotalol, Class 1a's
TCA, fluoxetine
Jervell-Lange-Neilsen, Romano-ward
166
Q

Antiplatelet mechanism of aspirin?

A

Inhibits the production of thromboxane A2

167
Q

Mechanism of action of clopidogrel

A

Antiplatelet - inhibits ADP binding to its platelet receptor via inhibition of P2Y12 receptor

168
Q

Mechanism of action of enoxaparin and fondaparinux

A

Activates antithrombin III, which in turn potentiates the inhibition of thrombin and coagulation factors Xa

169
Q

Mechanism of action of bivalirudin

A

Reversible direct thrombin inhibitor

170
Q

Mechanism of action of heparin

A

Activates antithrombin III, which in turn potentiates the inhibition of thrombin and coagulation factors Xa

171
Q

Management of NSTEMI/unstable angina?

A 
GRACE score (6 month mortality risk)
if > 1.5% clopidogrel for 12 months
if > 3% angiography within 96 hours + GIIb/IIIa antagonist
172
Q

Antipsychotics - side effects

A

Typicals - Antidopaminergic - EPSEs (ADAPT)
Atypicals - Antiserotoninweight gain
Either type
- Antihistaminic - drowsy
- Hyperprolactinaemia - galacttorhea, gynaecomastia, amenorrhoea, impotence
- Antiadrenergic - postural hypotension
- Antimuscarinic - dry mouth, const, blurred vision, retention, increased intraocular pressure
- Prolonged QT
- Neuroleptic malignant syndrome
Clozapine - agranulocytosis

173
Q

What drug can be used to lessen the dystonia sfx of antipsychotics?

A

Procyclidine (antimuscarinic)

174
Q

Side effects of tricyclic antidepressants?

A 
Sedative (esp amitriptyline)
Toxic in overdose
Arrhythmias 
Anticholinergic
Antiadrenergic
175
Q

Side effects of SSRIs?

A 
GI upset
Headache
Sexual dysfunction
Withdrawal symptoms (dizzy, lethergy, nausea, headache)
Safe in overdose
176
Q

Side effects of Lithium?

A

Narrow therapeutic range - check twice weekly then every 3 months
Excreted by kidney - check renal ftn before & every 6m
Can cause hypoTH - check TFTs before & every 6m
Teratogenic
Nausea, metallic taste, thirst, weight gain, oedema, tremor

177
Q

Define ‘opportunity cost’

A

The sacrifice in terms of the benefit forgone from not allocating the resources to the next best activity

178
Q

Define equity

A

Fairness or justice of distribution of costs and benefits

179
Q

Define economic evaluation

A

Comparative study of costs and effectiveness/benefits of different health care interventions
Analysed in terms of increments - eg are the incremental benefits of this new rx worth the incremental costs?
Simplest form is cost-effectiveness analysis, or can use cost-utility analysis

180
Q

What is cost-utility analysis?

A

Form of economic evaluation
Measures health in terms of QALYs (utility x life expectancy)
Incremental cost effectiveness ratio (ICER) must be <20,000 to be funded by NICE
ICER = incremental cost/incremental QALY = £X per QALY gained

181
Q

How do you calculate NNT?

A

1/Absolute risk reduction

182
Q

Valve most often involved in infective endocarditis

A

Tricuspid

183
Q

ECG signs of digoxin toxicity

A 
Reverse tick (down-sloping ST depression)
Short QT
184
Q

Enlarged heart on CXR without pulmonary oedema?

A

May be pericardial effusion - often a/w malignancy eg lung tumour

185
Q

Complications of Paget’s

A 
Bone pain
Pathological fractures
Nerve deafness
Spinal cord compression
High-output cardiac failure and
Osteosarcoma.
186
Q

What type of antiemetic are cyclising and promethazine?

A

Antihistamines - block h1 receptors in vomiting centre

Sfx - antimuscarinic, sedative

186
Q

Skin rashes caused by Malassezia?

A

Seborrhoeic dermatitis
Dandruff
Pityriasis versicolor

187
Q

What type of antiemetic are haloperidol, chlorpromazine, metoclopramide and domperidone?

A

Dopamine receptor antagonists - block da receptors in chemoreceptor trigger zone
Sfx - epse, sedation, long QT

187
Q

Causes of erythema nodosum?

A

infection: streptococci, TB, brucellosis
systemic disease: sarcoidosis, inflammatory bowel disease, Behcet’s
malignancy/lymphoma
drugs: penicillins, sulphonamides, combined oral contraceptive pill
pregnancy

188
Q

What type of antiemetic is ondansetron?

A

5ht3 receptor antagonist - block 5ht3 receptors in chemoreceptor trigger zone and gut
Sfx - qt prolongation, headache, flushing, constipation

188
Q

Rheumatoid arthritis - antibodies

A

RF, anti-CCF

189
Q

RA X ray changes

A

JS narrowing, periarticular osteopenia & erosions, soft tissue swelling, subluxation

190
Q

Treatment of RA & psoriatic arthritis?

A

Methotrexate + a DMARD (steroids for acute attacks)

191
Q

When dont you use DMARDS?

A

disease of the spine

192
Q

Features of sle?

A 
Hair loss
butterfly rash
discoid rash
livedo reticularis
photosensitivity
depression
glomerulonephritis
pleuritis
pericarditis
ulcers 
raynauds
antiphospholipd - CLOTS
seizures
Libman sacks endocarditis
193
Q

SLE antibodies

A 
ANA
Anti-dsDNA - best
Anti-Sm
Anti Ro, Anti La
Anti-histone - esp drug induced
Also low C3, C4
194
Q

Treatment of SLE

A

Cyclophosphamide, steroids, sun cream, hydroxychloroquine, NSAIDs, rituximab
Don’t use TNF blockers

195
Q

Pathology of Sjorgrens

A

Abnormal B cell activity - antibodies (Ro and La RF, ANA) attack exocrine glands

196
Q

Pathology of scleroderma

A

Overactive fibroblasts –> too much collagen –> vascular damage, inflammation

197
Q

Antibodies for systemic slerosis

A

Limited - anticentromere

Diffuse - Anti topoisomerase

198
Q

Clinical features of scleroderma

A

Cutaneous - linear and morphea skin fibrosis
Systemic
-Limited - CREST, pulm htn, renal crisis
-Diffuse - myocardial fibrosis, pulm htn, renal etc

199
Q

What is polyarteritis nodosa

A

Medium vessel vasculitis - necrotising arteritis –> aneurysms - a/w Hep B
Clinical features all related to ischaemia eg post prandial abdo pain, acute tubular necrosis
Arteriography –> aneurysms

200
Q

Risk factors for gout

A 
Alcohol Seafood meat (with purines in)
Male
Obesity
Diabetes
Thiazide diuretics
201
Q

Gout investigations

A

Joint aspirate - strongly negatively birefringent monosdium urate crystals
X -ray - erosions, punched out lesions, sclerosis

202
Q

Treatment of acute gout (and pseudogout)

A

NSAIDs, colchicine, steroids

203
Q

Prevention of gout

A

Allopurinol (xanthine oxidase inhibitor)

Lifestyle - low purine diet, look at drugs

204
Q

Pseudogout investigations

A

Joint aspirate - weakly positive rhomboidal calcium pyrophosphate crystals
X - ray - chondrocalcinosis

205
Q

Bisphosphonates - mechanism

A

Adhere to hydroxyapatite - inhibit osteoclasts

Alendronate is first line in osteoporosis

206
Q

Strontium ranelate - mechanism

A

Dual action - inhibit osteoclasts & promote osteoblasts

207
Q

Raloxifene - mechanism

A

SERM

208
Q

What is denosumab

A

Monoclonal antibody against RANK - used in osteoporosis

209
Q

What is teriparatide

A

Recombinant PTH - used in osteoporosis - anabolic mechanism

210
Q

Pagets - X-ray?

A

Sclerosis or lytic lesions, thickening of trabeculae, lose distinction of cortex

211
Q

Risk factors for osteomalacia

A

Low vit d or calcium or phosphate
Anticonvulsants
Renal tubular acidosis, renal failure
Malabsorption

212
Q

What is azothioprine

A

Purine analogue - inhibits DNA synthesis

213
Q

What is cyclosporin

A

Inhibits T lymphocytes and IL2

Monitor kidney function

214
Q

What are the 5ASA (aminosalicylates)

A

Sulfasalazine, mesalazine

215
Q

What hormone in pregnancy causes gestation diabetes?

A

Human placental lactogen

216
Q

Causes of microcytic anaemia

A

Fe deficiency, sideroblastic, thalassaemia

217
Q

What is sideroblastic anaemia

A

Can’t use iron in bone marrow –> get ring sideroblasts
Microcytic anaemia not responding to iron!
Low total iron binding capacity

218
Q

Causes of normocytic anaemia

A

Haemolytic anaemias

Chronic disease

219
Q

What is wrong with the beta chain in sickle cell

A

Replaced glutamic acid with valine

220
Q

Treatment of spherocytosis

A

Splenectomy

221
Q

What is myelodysplasia

A

Defect in stem cells –> bone marrow failure –> tends to evolve into AML
Old people

222
Q

Which pathway does prothrombin time measure

A

Extrinsic - used for warfarin monitoring (INR)

223
Q

Which pathway does APTT measure

A

Intrinsic - used for monitoring heparin - increased in haemophilia & VW disease

224
Q

How do GPIIb/IIIa antagonists work?

A

Block binding of fibrinogen to platelets

225
Q

How does heparin work

A

Inactivates thrombin and factor Xa

226
Q

How does clopidogrel/tacegralor work

A

P2y12 receptor inhibitors - block platelet activation

227
Q

How do alteplase, retaplase etc work

A

Recombinant tissue plasminogen activator - activates plasmin from plasminogen - plasmin breaks down fibrin

228
Q

Features of PKD?

A

Hypertension, infections, abdo pain, compression, hepatic cysts, berry aneurysms

229
Q

Where does renal cell carcinoma arise?

A

Proximal tubule

230
Q

Causes of CKD

A 
Congenital disease eg pkd
Glomerular disease
vascular disease
tin
urinary obstruction
231
Q

Complication of CKD

A 
Polyuria
Itching
Gout
Hyperprolactinaemia
Polyneuropathy
ED, amenorrhoea
Anaemia
renal osteodystrophy
uraemic encephalopathy/pericarditis
232
Q

How do you treat someone with vit d deficiency and CKD?

A

Calcitriol (activated vit d)

233
Q

What do HHV 6 & 7 cause

A

Roseola infantum

234
Q

What do the paramyxoviridae cause?

A

Measles & mumps

235
Q

What are cestodes?

A

Tapeworms - from pork and beef

236
Q

What are nematodes?

A

Roundworms - hookworm, pinworm, threadworm, whipworm

237
Q

What are trematodes?

A

Schistosomiasis

238
Q

Treatment of schistomiasis?

A

Praziquantel

239
Q

What are adrenaline & noradrenaline

A

Direct sympathomimetics
Adrenaline –> act on beta and alpha - used in anaphylaxis, in CPR, with local anaesthetic, in croup
Noradrenaline –> vasoconstriction via alpha 1 receptors - used to increased systemic vascular resistance

240
Q

Treatment of whooping cough

A

Erythromycin

241
Q

What are phenylephrine and metaraminol?

A

Alpha agonists - vasoconstriction - sympathomimetics - like noradrenaline but less direct

242
Q

Treatment of status epilepticus

A

Ensure safety, ABC, high flow o2
Give buccal midazolam, rectal diazepam or iv lorazepam –> up to 2 doses –> then iv phenobarbitol or phenytoin
If refractory –> iv propofol or thiopentol

243
Q

What is ephedrine

A

Mixed alpha and beta agonist sympathomimetic

244
Q

What is dobutamine

A

Directly acts on beta1 receptors (heart) –> so is an ionotrope - used in heart failure, pulmonary oedema

245
Q

Timilol?

A

Decreases aqueous secretion of ciliary body - used in primary open angle glaucoma

246
Q

What are alpha 1 receptors?

A

Causes vasoconstriction of non vital organs & contraction of bladder sphincter (sympathetic nervous system)

247
Q

What are beta 1 receptors?

A

Increase contraction of cardiac muscle (sympathetic nervous system)

248
Q

What are beta 2 receptors?

A

Relax smooth muscle of bronchus, vasculature and uterus (sympathetic nervous system)

249
Q

What is digoxin?

A

Positive ionotrope - used in heart failure and AF

250
Q

How do nitrates work?

A

Increase cyclic GMP
Vasodilates veins –> reduce preload (also vasodilate coronary arteries)
GTN - short acting
Isosorbide mononitrate - long acting

251
Q

How verapamil & diltiazem work?

A

Block AV node

252
Q

Histamine antagonists

A

H1 = antiallergy
Sedating - chlorphenamine, promethazine, cyclizine (also antiemetics)
Non-sedating = cetirizine, loratidine

H2 = parietal cells
Ranitidine, cimetidine

253
Q

Pathophysiology of paracetamol overdose

A

Paracetamol usually metabolised by liver conjugation
In overdose the liver conjugation becomes inundated so paracetamol is metabolised by an alternate pathway, creating toxic NAPQ - this is inactivated by glutathione
When glutathione stores are depleted, NAPQ causes necrosis of liver and kidney cells
Rx - N acetyl cysteine

254
Q

Carbon monoxide poisioning mgmt

A

High flow oxygen

sats are normal

255
Q

TCA overdose - mgmt

A

Charcoal, gastric lavage

IV diazepam, IV sodium bicarbonate

256
Q

Aspirin overdose - mgmt

A

Charcoal, gastric lavage
Urinary alkalinisation
Haemodialysis

257
Q

Ethylene glycol poisoning - mgmt

A

ethanol or fomepizole - inhibit alcohol dehydrogenase

258
Q

Digoxin toxicity - mgmt

A

FAB antibody

259
Q

Insecticide poisoning - mgmt

A

Atropine

263
Q

How to prove someone negligent?

A 
Must be a duty of care
Must be a breech of duty of care
Are their action supported by others?
Did pt come to harm?
Did the breech cause the harm?
264
Q

Effect of lithium on thyroid function?

A

Inhibits production and release of T3 and T4 –>hypothyroidism

265
Q

What can cause hypernatraemia with a high urine output?

A

Osmotic diuresis

Impairment of ADH function (diabetes insipidus)

266
Q

Causes of diabetes insipidus

A

Nephrogenic - lithium, CKD, ATN, hypercalcaemia, hypokalaemia
Cranial - trauma, infection, tumours

267
Q

Diagnosis of diabetes insipidus

A

Water deprivation - failure to raise urine osmolality to 650 mmol/kg
Give desmopression - if cranial, osmolality will rise to >650, if nephrogenic, it won’t

Medicine Finals (5 decks)

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