CMS Flashcards

Question

if patient in shock i.e. lost excessive amounts of blood

Answer 1

immediate - stop bleeding via vascular, platelet & plasma responses i.e. smooth muscle constriction & platelet adhesion & aggregation by endothelium short term - BP restored by vasoconstriction produced by thromboxane A2 & ADP medium term - restore volume of fluid by activating RA system so kidney absorbs more water & salt to keep blood volume up, ADH has similar effect as well as vasopressin effects constricting blood vessels long term - replace constituents of blood

Answer 2

haemophilia A - factor VIII deficiency haemophilia B - factor IX deficiency

Answer 3

sex linked recessive factor VIII deficiency carriers/mild = DDAVP used to increase levels of factor VIII / oral tranexamic acid (antifibrinolytic agent) moderate / severe recombinant = factor VIII should be used to replace factor lost

Answer 4

sex linked recessive factor IX deficiency carriers/mild = oral tranexamic acid as DDAVP will not increase factor IX levels moderate / severe = only use of recombinant factor IX

Answer 5

reduced factor VIII levels & reduced platelet aggregation autosomal dominant disease characterised by deficiency of von willebrands factor tx = DDAVP to increase factor VIII or oral tranexamic acid

Answer 6

depends on severity carriers / mild can be seen at GDP with review every 2yrs - observed for 2-3hrs following XLA, biopsy etc moderate / severe should be seen in hospital setting - observed overnight IBD only undertaken in hospitals do not give NSAIDs i.e. aspirin so this will inhibit platelet aggregation & increase bleeding

Answer 7

increases risk of clot development inherited = protein C/S deficiency, factor V leiden & antithrombin III deficiency acquired = DVT, OCP, surgery trauma, cancer, pregnancy

Answer 8

1. mild = blood results normal so ptx treated as normal 2. moderate = platelet count >100 so shouldn't be any issue with tx but local measures for haemostasis may need to be accounted for 3. severe = lack of many clotting factors, platelet count <100 so XLA & invasive procedures should be undertaken in a hospital setting

Answer 9

want consistent INR of 2-4 it will antagonise vit K which is required for synthesis of factors 2 7 9 10, protein C & S

Answer 10

potentiating drugs = ACE inhibitors, antibiotics, NSAIDs inhibiting drugs = epilepsy drugs & alcohol

Answer 11

INR must be checked 48hrs before tx, if unstable check 24hrs, avoid IBD if possible, if tx of warfarin is to be stopped for tx wait 72hrs after (12hrs if heparin)

Answer 12

both of these are irreversible for the life of the platelet which is 7 days if low dose aspirin & clopidogrel used separately there is no effect on post op bleeding but if used together there will so stop 7 days prior to surgery / invasive procedure

Answer 13

irreversible - age, sex, family history behavioural - smoking, alcohol, diet, exercise, obesity factors managed by drugs - hypertension, hyperlipidaemia, diabetes, stress drugs that can increase risk - corticosteroids, OCP, sympathomimetrics i.e. adrenaline

Answer 14

1. anti-platelet 2. anti-arrhythmics 3. lipid lowering these help stop build up of atheroma & help keep the rhythm of the heart under control, help to prevent further hypertension, heart arrhythmias & prevent infarction

Answer 15

e.g. aspirin & clopidogrel widespread atherosclerosis causes more platelet aggregation which can narrow or occlude blood vessels leading to ischaemia / infarction so these drugs are used to decrease total peripheral resistance to decrease BP

Answer 16

e.g. statins inhibit cholesterol synthesis in liver reducing blood cholesterol & LDL levels to reduce further build up of atheroma, help to stabilise TPR keeping BP down these can interact with antifungals & cause myositis

Answer 17

e.g. amiodarone bock beta receptors in heart preventing increase in heart rate thus reducing cardiac output these can cause postural hypotension due to decreased heart rate & can worsen heart failure, will also block beta receptors in lungs making asthma more difficult to treat

Answer 18

1. diuretics 2. anti-arrhythmics 3. nitrates 4. calcium channel blockers 5. angiotensin converting enzyme inhibitors these drugs help reduce BP thus helping to prevent symptoms of disease & prevent further disease occurring

Answer 19

e.g. thiazide / loop - furosemide thiazide; inhibit NaCl cotransporter in DCT of kidney decreasing Na reabsorption so increased fluid passed as urine e.g. chlorothiazide loop; inhibit NaClK cotransporter in ascending loop of henle overall reduce blood plasma volume thus reducing cardiac workload & BP helping reduce symptoms of heart failure side effects are Na/K imbalance if not monitored properly, can cause gout

Answer 20

e.g. glyceryl trinitrate work by releasing nitrous oxide which causes vasodilation throughout the body, veins supplying heart are dilated reducing preload, resistance arteries will dilate reducing workload & oxygen consumption & collateral coronary artery supply will be dilated reducing angina pain used as a spray sublingually in emergency

Answer 21

e.g. amlodipine block calcium channels in smooth muscle including the heart slowing conduction (calcium used to lengthen action potentials), causes vasodilation in peripheral blood vessels, both of these decrease BP side effect - gingival hyperplasia

Answer 22

e.g. prils inhibit conversion of angiotensin I to angiotensin II which prevents aldosterone release from medulla of adrenal gland meaning that aldosterone will not be used to resorb salt & water leading to reduced salt & water retention which reduces BP side effects - hypotension & cough

Answer 23

deficient blood supply to tissue which can lead to hypoxia / necrosis can be due to atheroma, embolism or thrombosis ischaemia leads to infarction over time

Answer 24

build up of plaque due to accumulation of lipids, smooth muscle proliferation & formation of fibrous tissue predisposed by hyperlipaemia, smoking, hypertension, diabetes atheroma leads to arterial narrowing causing angina / intermittent claudication can cause increased thrombosis which can lead to ischaemia / infarction can weaken arterial walls causing aneurysm

Answer 25

formation of solid mass from blood constituents in vascular system predisposed by atheroma, turbulent blood flow, hypercoagulable blood

Answer 26

vascular transfer of a substance by blood which becomes stuck in a blood vessel distant from the origin often caused by thromboembolism thrombus from left side of heart / arteries break off it can cause ischaemia / infarction due to blood flow obstruction thrombus formed in DVT can cause focal pulmonary infarction / may obstruct main pulmonary arteries from right side of heart causing sudden death

Answer 27

stable = cardiac arteries become ischaemic so not enough oxygen supplied heart under exertion unstable = randomly occurs with symptoms sometimes mimicking MI, may be rapid deterioration

Answer 28

central crushing autonomic nerve pain which is relieved by rest sometimes a hyperdynamic circulation

Answer 29

ECG - typically normal but on pain often a raised or lowered ST segment, may see raised ST if previous MI angiography - to view occlusion or narrowing of coronary arteries echocardiogram

Answer 30

tx required as over time it will lead to infarction best action is to modify risk factors i.e. stop smoking, improve diet & increase exercise drug therapy - anti platelet i.e. aspirin to prevent platelet aggregation on atheroma, Ca channel blockers, diuretics, beta blockers, ACE inhibitors to reduce BP, decreasing amount of atherosclerosis forming & reducing load of heart, nitrates e.g. GTN to reduce preload & dilate coronary arteries surgical therapy - CABG or angioplasty with stenting

Answer 31

peripheral vascular disease i.e. ischaemia of the tissues named intermittent claudication & affects lower limbs pain on exertion & relived by rest

Answer 32

complete blockage of 1 of the coronary arteries leading to functional limitation or death ST segment elevation and after a Q wave will be present symptoms - pain, nausea, paleness, sweating signs - increased troponin level

Answer 33

get to hospital as soon as possible prescribe aspirin to prevent platelet aggregation, beta blockers & Ca channel blockers to slow heart rate reducing O2 demand, ACE inhibitors & diuretics to reduce heart load by reducing BP angioplasty & stenting preferred to thrombolysis as this is only effective when given early and will cause all clots to break down causing bleeding so contraindicated in liver disease, severe hypertension & pregnancy again modify risk factors

Answer 34

infarction to cerebral arteries in the brain caused by embolism from atheroma or cerebral bleed

Answer 35

central crushing chest pain can radiate to jaw may struggle to get up stairs in dental surgery LA with adrenaline may cause angina attack due to increased heart rate if accidentally injected into vein

Answer 36

p wave - atrial depolarisation qrs complex - ventricular depolarisation t wave - ventricular repolarisation during MI ST is raised and in angina it is lowered

Answer 37

no p wave present high heart rate with irregular beats same as in MI

Answer 38

shockable rhythm irregularly irregular

Answer 39

drug induced by beat blockers heart block

Answer 40

pacemaker caution when using ultrasonic scaler as risk of electrical interference

Answer 41

normal = 120/80mmHg hypertension = 140/90mmHg systolic = pressure when heart pushes blood out diastolic = pressure when heart rests between beats if systolic high there is increased stroke risk due to high BP potentially causing aneurysm & rupturing in cerebral veins & arteries if diastolic high it causes more problems as heart will have to push harder against already high pressure

Answer 42

1. essential hypertension - no specific cause but thought to be due to how endothelial cells react to different stimuli i.e. different genetics cause a different response 2. renal artery stenosis (glomerulonephritis) - kidney arteries become blocked / damaged due to atherosclerosis or thromboembolism causing less water to be excreted increasing BP 3. endocrine tumour - release different hormones increasing BP e.g. phaeochromocyte tumours cause sudden adrenaline release, conn's syndrome causes aldosterone release & cushing's causes cortisol release

Answer 43

often go unnoticed make get TIAs i.e. mini stroke where cerebral arteries will be temporarily blocked by an embolism which is broken down within 24hrs & neurological function returns

Answer 44

can lead to increased atheroma, MI, stroke, PVD & renal failure as heart will have to work harder against increased BP causing left ventricular hypertrophy which will increase risk of left heart failure especially if heart can no longer pump against increased BP

Answer 45

aim to lower BP to <140/90 by modifying risk factors / pharmacological intervention i.e. diuretics, beta blockers, ca channel blockers, ACE inhibitors

Answer 46

output of heart not capable of meeting demands of the tissues; can be: 1. low output failure i.e. problem with heart 2. high output failure i.e. problem with the body as a whole

Answer 47

heart is pumping correctly & should be supplying tissues but due to issues with the rest of the body the tissues are not receiving enough oxygen to meet their demands. 2 main causes = 1. anaemia - not enough haemoglobin in blood to transport oxygen to tissues 2. thyrotoxicosis - increased thyroxine hormone produced which increases demands of tissues

Answer 48

heart is failing as an organ, not pumping enough blood to keep up with demand; defects include; MI & valve disease have R, L, congestive (both) failure, often it will start with L then lead to R

Answer 49

multifactorial disease: - heart muscle disease; includes MI & myocarditis, decreased cardiac output as heart has functional limitation - pressure overload; diastolic hypertension; heart has to pump harder against already high BP to force blood into peripheral tissues, aortic stenosis; narrowing of aorta so heart uses more pressure - volume overload; mitral / aortic valve incompetence the efficiency of heart as a pump will be greatly reduced - arrhythmias; irregular heart rhythm will lead to decreased efficiency of heart i.e. atrial fibrillation - drugs; beta blockers can decrease HR leading to low output failure

Answer 50

LHS - problems with lungs & systolic BP affected causing dyspnoea (fluid in lungs causing breathlessness especially lying down), orthopnoea, tachycardia, low BP/volume/pulse RHS - increase venous pressure and so diastolic BP leading to swollen ankles, ascites, raised JVP, tender enlarged liver & poor GI tract absorption tends to be left affected first

Answer 51

underlying cause must be treated in chronic failure inotropes e.g. digoxin taken to increase heart function with negative inotropes e.g. beat blockers stopped diuretics, ACE inhibitors, nitrates can be used to reduce BP & heart load in acute heart failure send to hospital where it is treated with oxygen, morphine & furosemide

Answer 52

mitral (bicuspid) - left tricuspid - right LAB RAT pulmonary - right aortic - left

Answer 53

issue with valves of heart left more likely to be affected due to higher pressure needed; these are the aortic & mitral valves

Answer 54

1. usually stenosis of valve so it has narrowed & less blood flows through it 2. congenital bicuspid aortic valve where tricuspid has only 2 cusps not 3 3. after an MI there could be papillary muscle rupture leading to valve incompetence 4. rheumatic fever - can lead on to rheumatic heart disease which can cause valve damage; these ptx can require antibiotic prophylaxis

Answer 55

valve replacement therapy

Answer 56

infection of the endocardium usually the valves where there are surface irregularities, microbial colonisation may occur due to turbulence of blood leading to thrombus formation; likely to aggregate bacteria (usually oral bacteria) which enter through bleeding gingivae or invasive procedures

Answer 57

- acquired valvular heart disease - valve replacement - congenital heart disease - hypertrophic cardiomyopathy - previous endocarditis

Answer 58

40-50% cases oral streptococci also s.aureus & c.albicans

Answer 59

used to give antibiotic prophylaxis but risk of anaphylaxis high so ptx must maintain excellent OH instead AB prophylaxis is 3g amoxicillin given orally 1hr before tx

Answer 60

average pulse = 60-100bpm average respiratory rate = 12-18 breaths/min

Answer 61

symptoms - cough, wheeze (expiratpory noise), stridor (inspiratory noise), dyspnoea (distress on effort breathing) signs - resp rate increased, air entry to lungs (is it symmetrical?), percussion note, is fluid present

Answer 62

- examine sputum from ptx - chest radiograph - PEFR to investigate flow rate - FEV1 to test expiratory volume - bronchoscopy - VQ scan

Answer 63

MDI - meter dose inhaler must be used with spacer device spacer device will help prevent c.albicans settling in oral mucosa causing oral candidosis

Answer 64

1st drug used in stepladder against obstructive airway diseases treat acute bronchial constriction by relaxing smooth muscles in bronchioles onset is 2-3mins route of admin = oral, IV, inhalation e.g. salbutamol / terbutaline if ptx on beta blockers this will not be an effective drug as beta blockers are non selective so will oppose the action of the beta 2 agonist

Answer 65

2nd drug used in stepladder against obstructive airway diseases will counter immune reaction instead of just opening airways i.e. in asthma the mucous production, inflammation & constriction of airways will all be countered admin = topical / systemically if dose >800ug spacer must be used e.g. beclomethasone / fluticasone

Answer 66

used in conjunction with corticosteroids in later stage respiratory failure slower onset but lasts 12-15hrs so is used to PREVENT acute bronchial constriction, must be inhaled & used with steroid as long acting beta 2 agonists increase the risk of heart attack but steroid will reduce it e.g. salmeterol / formoterol

Answer 67

will block muscarinic nerve transmission in autonomic nerves & will reduce basal tone of bronchioles and may be useful in COPD ptx

Answer 68

GA uses benzodiazepines which are a respiratory depressant so this can make respiratory failure more likely

Answer 69

bronchial hypersensitivity reaction causing reversible airflow obstruction of smaller airways leading to difficulty breathing; 3 processes: 1. bronchoconstriction 2. inflammation 3. excessive mucous production

Answer 70

stepladder: 1. short acting B2 agonist 2. low dose inhaled corticosteroid 3. high dose inhaled corticosteroid 4. long acting B2 agonist with inhaled corticosteroid 5. oral steroid

Answer 71

2 process disease that is irrerversible: 1. emphysema - destroys alveoli forcing adjacent alveoli to enlarge and fill gap which lowers SA for gas exchange, this plus thickened alveolar mucosal barrier, blood becomes less oxygenated & respiratory failure occurs over time 2. bronchitis - cough with sputum production on most days for 3mths of yr for 2 consecutive yrs, will restrict size of airways as increased mucous production with inflamed walls

Answer 72

type 1 = failure of oxygenation as hypoxaemia (<90% O2 saturation in blood) due to poor ventilation or diffusion abnormality caused by thickening of alveoli; causes VQ mismatch & death type 2 = failure of ventilation as hypercapnia (high CO2), narrowing or blockage of airways & breathing out will be a problem leading to inadequate CO2 removal and so death

Answer 73

if chronic COPD oxygen given with care as if ptx resp rate driven by hypoxia then high levels of O2 detected from O2 delivery system then it can cause ptx to stop breathing

Answer 74

inherited autosomal recessive disorder of CFTR gene on chromosome 7 that affects the lungs - excess production of sticky mucous & pancreas - malabsorption of nutrients & disorder of Cl - channels

Answer 75

cough with repeated chest infections (pseudomonas staphylococci), poor weight gain, prolonged diarrhoea

Answer 76

physio medication - bronchodilators, steroids to open airway & reduce inflammation / antibiotics to reduce chest infection frequency, replacement of pancreatic enzymes in final stages heart & lung transplant required

Answer 77

difficult to diagnose, main risk is smoking & majority of these will be malignant so metastasise: 1. squamous cell carcinoma 2. large cell 3. small cell 4. adenocarcinoma

Answer 78

airway obstructed for about 10s while sleeping as he tone to airway muscles will drop can cause drowsiness during day, increases risk of MI 2 types = obstructive sleep apnoea - likely to snore & central sleep apnoea tx = mandibular advancement devices to pull bottom jaw forwards to hopefully eliminate blocking of airway

Answer 79

secretions of lactoferrin, salivary IgA, cilia, neutrophils, normal flora

Answer 80

consolidation of lung parenchyma meaning it is no longer compressible due to fluid being present in the active areas of the lung i.e. alveoli & there is inflammation of the gas exchange areas with intense inflammatory infiltrate

Answer 81

sudden onset, fever, malaise, rigors, SoB, cough with purulent sputum (pus which is green / yellow, consolidation of lungs in chest x ray

Answer 82

1. community acquired - step pneumoniae, haemophilus influenzae, staph aureus 2. atypical - chlamydophilia pneumoniae, mycoplasma pneumoniae 3. legionella - inhalation of contaminated aerosols i.e. in the dentist

Answer 83

highest worldwide cause of Addison's disease risk factors = contact with another person with TB, HIV, IV drug abuse, alcoholism, residency in prison

Answer 84

chronic cough with haemoptysis (coughing up blood), weight loss & night sweats plus chest xray, sputum culture & if high risk ptx or not tx = multiple drug therapy over time

Answer 85

1. acute = during winter & is viral 2. chronic = productive cough on most days over 3 months in 2 successive years predisposing factors for bronchitis = smoking, infections, air pollution & allergies, usually viral or bacterial agents involved

Answer 86

common bacteria in this is strep pyrogenesis group A, complications are: 1. suppurative - retropharyngeal abscesses, sinusitis, otitis media, cervical lymphadenitis 2. non suppurative - scarlet fever, strep toxic shock, glomerulonephritis, rheumatic fever

Answer 87

highly infectious epidemic RNA virus with type a, b, c but only type a will undergo major changes necessary to form a pandemic highest mortality in elderly

Answer 88

genetic disease where there is sensitivity to gluten due to alpha gliadin in it & this protein will react with jejunum causing an inflammatory reaction causing villus atrophy (may be to extent that is clinically visible) & this causes insufficient nutrient absorption

Answer 89

malabsorption of iron, folate, B12 (anaemia) & fat weight loss lassitude (lack of energy) weakness, abdominal pain diarrhoea steatorrhea dysphagia

Answer 90

do jejunal biopsy check haematinics check if they respond to gluten free diet

Answer 91

risk factors = smoking, age, obesity, alcohol, ulcerative colitis, intestinal polyps often no symptoms so usually diagnosed by routine screening i.e. FOB, endoscopy, CT/MRI if poorly differentiated survival rate is low, if metastasis to liver survival as low as 5%

Answer 92

caused by immunological / psychological factors, smoking 2 main types: 1. crohn's 2. ulcerative colitis

Answer 93

continuous inflammation, colon always involved, abscesses in mucosa but below the serosa will be normal, may develop into carcinoma over time so must be monitored

Answer 94

inflammation discontinuous, will affect whole of GI tract not only the colon, mucosa cobbled & fissured with inflamed serosa, oedema & granulomas i.e. OFG (lip swelling, angular cheilitis, cobblestoning of lips & cheeks, gingivitis, ulceritis)

Answer 95

both diseases will include diarrhoea, abdominal pain, rectal bleeding as they involve the colon crohns - includes other areas of GI tract so can have small bowel disease causing pain, obstruction & malabsorption, can also lead to anaemia, OFG

Answer 96

systemic steroids to reduce inflammation - infliximab (stop inflammation), azathioprine (immunosuppression) & sulphasalazine (reduce inflammation), surgery as a last resort

Answer 97

affects stomach upwards 3 main categories of disease: 1. oral disease 2. oesophageal disease 3. gastric disease

Answer 98

2 categories: 1. eliminating acid formed (antacids) 2. reducing acid secretion stomach acid produced in parietal cells when there is a trigger for acid production; the 3 triggers are: 1. acetylcholine 2. gastrin (released when food in stomach) 3. histamine - H2 receptor agonists will block this receptor

Answer 99

reduce stomach acid production by preventing histamine activation of stomach acid production but there are 2 other pathways present for production of acid so it is not that effective

Answer 100

will target proton pump at top of parietal cells meaning it will effectively block all acid production in the stomach reducing reflux

Answer 101

1. recurrent oral ulcerations - often idiopathic but can have pathological causes 2. OFG - most often if they have crohn's 3. lichen planus - inflammatory disease of skin & mucous membranes

Answer 102

1. dysmotility - issues with muscle tissue caused by fibrosis from acid reflux 2. dysphagia - difficulty swallowing due to blockage / compression of oesophagus 3. GORD - defective lower oesophageal sphincter leading to impaired lower cleaning & gastric emptying causing acid to leak into oesophagus; will cause ulcerations, inflammation & metaplasia (change from oesophageal mucosa to gastric mucosa)

Answer 103

burning in epigastric region, worse when laying, bending & birth may cause dysphagia, stricture, dysmotility, GI bleeding (leading to anaemia)

Answer 104

recurrent acid reflux into lower oesophagus causing metaplasia of the lower oesophageal lining into gastric type mucosa associated with malignant change and may change to adenocarcinoma over time

Answer 105

name for disease of any acid affected site e.g. increased stomach acid will cause oesophageal / duodenal ulceration; if there is normal acid secretion it may cause ulceration if there is reduced protective barrier, in this situation there is often H.pylori involvement NSAIDs & steroids can increase risk of PUD

Answer 106

this bacterium will cause inflammation of stomach lining leading to ulcerations, these will break down the wall due to acid secretion & if severe can lead to bleeding & perforation even lymphoma of stomach tx is via triple therapy - 2 antibiotics (amoxycillin & metronidazole) and a PPI

Answer 107

often asymptomatic can cause epigastric burning pain just before / after a meal relieved by alkaline food / vomiting investigated via endoscopy

Answer 108

if reversible, disease can be changed by lifestyle i.e. stopping smoking, small regular meals or by drugs may require surgical intervention i.e. stricture

Answer 109

clinical appearance of bilirubin pigmentation in skin & other organs will cause itching & ptx known to be icteric

Answer 110

enterohepatic process: in this, liver haem is conjugated and made water soluble for excretion. it will initially be secreted into the bile however, some is reabsorbed & released as urobilinogen in the urine & in jaundice this process is disrupted; it can pre hepatic, hepatic or post hepatic

Answer 111

jaundice due to problems before the liver i.e. - increased haem load due to excess RBC or excess breakdown can be due to haemolytic anaemia, post transfusion if bad match, neonatal due to mother's blood type not matching baby's

Answer 112

failure of the hepatic cells themselves due to liver failure so cirrhosis or drug induced liver dysfunction or may even be due to hepatitis if there is failure of secretion then the urine will be dark as conjugated bilirubin is dark & faeces will be lighter

Answer 113

problem after the hepatocytes usually caused by an obstruction - if obstruction in hepatic biliary system it could be due to primary biliary sclerosis - if extrahepatic it could be due to gall stones or pancreatic carcinoma compressing the common bile duct or due to pancreatitis which will cause inflammation & swelling that will compress ; usually from CF, alcoholism

Answer 114

yellow discolouration due to deposition of excess unconjugated bilirubin throughout the body if stool is pale & urine is dark there is post hepatic jaundice as conjugated bilirubin in urine if due to haemolytic anaemia the stool & urine will be normal

Answer 115

formed in gall bladder & may block biliary tree causing obstructive jaundice stones cause cholecystitis (inflammation of gall bladder itself), inflammation of biliary tree, pain in tip of shoulder (radiation from diaphragm as they are both phrenic nerve)m, right side abdominal pain

Answer 116

identify cause & treat it

Answer 117

if baby born under high amount of trauma this will cause increased haem breakdown so there is more in blood & due to poor liver function of neonate it will not break down bilirubin correctly causing jaundice blue light can be used to break it down can cause kernicterus

Answer 118

supplied by hepatic artery & portal vein with connecting bile ducts forming a portal triad which then connects to the hepatic vein output the further away a hepatocyte is away from the blood vessel, the more likely it will be damaged due to its low oxygen concentration so it will not regenerate easily

Answer 119

most often caused by paracetamol poisoning can cause sudden loss of liver function & rapid death due to bleeding & encephalopathy (too much nitrogen in blood)

Answer 120

occurs over a no of years causes loss of synthetic function of liver & metabolic function; this means plasma proteins & clotting factors will not be produced tested via INR (time it takes prothrombin to be converted to thrombin) dose of drugs must be carefully controlled as no longer adequate FPM detoxification will not longer occur nor conjugation of RBC breakdown products i.e. jaundice occurs causes = cirrhosis, primary liver cancer, secondary liver cancer from metastasis or hepatitis

Answer 121

fibrosis of liver leading to nodule formation end stage is irreversible often no symptoms other than larger / smaller liver but may be acute bleeding, hypertension, jaundice, oedema with ascites, encephalopathy, spider naevi

Answer 122

inflammation of liver 1. acute = acute liver failure, non specific symptoms i.e. nausea, malaise, hepatomegaly, jaundice, prolonged bleeding due to not enough clotting factors & elevated bilirubin 2. chronic = diagnosed by inflammation over 6mths as progressive injury with liver cell loss, fibrosis & regeneration over a long period of time; will lead to cirrhosis main particle in hep B is dane particle

Answer 123

viral infections, drugs, autoimmune disease, alcohol, metabolic disease, biliary disease i.e. gall stones or idiopathic

Answer 124

- must liaise with physician - antifungals avoided - NSAIDs will increase bleeding risk so paracetamol best analgesic - sedatives will have prolonged effect so IV sedation must be avoided - reduced clotting factor synthesis so liaise with haematologist - reduced plasma transport protein synthesis so drug binding is reduced so need to reduce drug dose - reduced gamma globulin synthesis so ptx will be more prone to infection *no issues with LA as LA broken down in plasma, not liver

Answer 125

disease associated with dysfunction of a hormone secreting gland 2 different forms of failure: 1. control failure 2. gland failure

Answer 126

hormones secreted by hypothalamus & transfer to anterior pituitary to trigger secretion of hormones here transferred via hypothalamic pituitary portal vessels hormones released inc: adrenocorticotrophic, thyroid stimulating, growth these are kept at homeostasis via negative feedback

Answer 127

over secretion - acromegaly under secretion - growth failure dental aspect of acromegaly = enlarged tongue with interdental spacing

Answer 128

produces thyroxine which will act to increase metabolic rate of all cells

Answer 129

excess thyroxine primary = problem affecting the gland not pituitary secondary = rare causes = grave's disease, toxic multinodular goitre, toxic adenoma, pituitary tumour (rare)

Answer 130

autoimmune disease - most common cause of hyperthyroidism caused by autoantibodies stimulating thyroid stimulating hormone receptor on thyroid gland so release thyroxine specific symptoms = inflamed scleral blood vessels, proptosis, periorbital oedema

Answer 131

symptoms - hot sweaty skin, weight loss, diarrhoea, palpitations, muscle weakness, heat intolerance, irritability signs - tachycardia, atrial fibrillation, increased BP, tremor, eyelid retraction

Answer 132

generally involved blocking thyroid gland / thyroxine carbimazole will block thyroid gland, thyroxine then must be supplemented as hypothyroidism develops radioiodine tx can be used; kills off part of thyroid gland

Answer 133

lowered amounts of thyroxine produced so basal metabolic rate of cells is reduced primary = more common i.e. hashimoto's thyroiditis, radioiodine tx, iodine deficiency secondary = very rare if thyroxine not produced this leads to increased amounts of thyroid stimulating hormone to be released from anterior pituitary which leads to hypertrophy of the thyroid gland

Answer 134

autoimmune disease present with goitre symptoms = tiredness, cold intolerance, weight gain, constipation, goitre, angina signs = slow pulse, bradycardia, hyperlipidaemia, goitre, delayed reflex response tx = T4 tablets

Answer 135

3 main molecules tested for = TSH, T3, T4 primary hyperthyroidism (problem with gland itself) = low TSH (not stimulated by pituitary) & high T3 secondary hyperthyroidism = raised TSH, high T3 primary hypothyroidism = problem with the thyroid gland so high TSH but low T4 secondary hypothyroidism = low TSH & T4 due to problems with anterior pituitary itself

Answer 136

mineralocorticoid produced in zone glomerulosa of adrenal gland cortex; involved in RAAS if BP too low it is detected in juxtaglomerular apparatus leading to renin synthesis & release which converts angiotensin to angiotensin I which is converted by ACE to angiotensin II in the lungs; this stimulates the adrenal cortex to produce aldosterone which acts to increase Na+ resorption water retention & increases K+ loss which will act to increase BP

Answer 137

ACE inhibitors - inhibit conversion of angiotensin I to angiotensin II lowering BP, has side effects of cough, angiooedema (fat tongue), oral lichenoid drug reactions

Answer 138

natural glucocorticoid that is an antagonist to insulin meaning it causes gluconeogenesis, fat & protein breakdown, lowers immune reactivity of ptx (anti-inflammatory), decreases chemotaxis of neutrophils so less of them involved in inflammatory reactions, inhibits bone synthesis which over time can lead to osteoporosis, will increase BP as it is chemically related to aldosterone. it is controlled by CRH & ACTH

Answer 139

as anti-inflammatory drug or for immunosuppression however can cause adrenal gland atrophy because there no longer will be stimulation of it from the anterior pituitary gland so it is no longer needed

Answer 140

hypertension type 2 diabetes cataracts hyperlipidaemia (accelerated atherosclerosis) decreased chemotaxis of neutrophils so increased infection risk osteoporosis due to inhibition of bone synthesis

Answer 141

increased glucocorticoid & mineralocorticoid synthesis leading to conn's syndrome and cushing's syndrome

Answer 142

increased aldosterone production leading to hypertension & hypokalaemia with hypernatremia

Answer 143

main cause is cushing's disease which is a pituitary tumour other causes - adrenal adenoma or ectopic ACTH production

Answer 144

diabetes features i.e. polyurea & lethargy poor resistance to infection hirsutism (bearded ladies) amenorrhea increased ACTH leading to increased skin pigmentation

Answer 145

moon face buffalo hump thin skin that is easy bruised

Answer 146

decreased amount of glucocorticoid & mineralocorticoid released from adrenal gland caused by compression of pituitary from another adenoma or sheehan's syndrome or hypovolaemic shock

Answer 147

primary cause of hypofunction being gland failure; due to autoimmune gland destruction, infection or infarction

Answer 148

signs - postural hypotension due to depletion of water & salt as there is absence of aldosterone, weight loss, lethargy, hyperpigmentation symptoms - weakness, anorexia, loss of body hair in females

Answer 149

in 2ndary hyperfunction - increased ACTH & cortisol in primary hyperfunction - low ACTH & high cortisol in 2ndary hypofunction - low ACTH & low cortisol in primary hypofunction - high ACTH & low cortisol

Answer 150

type 1 - body does not produce enough insulin type 2 - cells do not respond to insulin that is produced (insulin resistant)

Answer 151

produced by beta cells in islets of langerhans in the pancreas released in response to high blood glucose levels & will act to lower concentration occurs by facilitating glucose uptake into muscle cells & adipocytes (NOT LIVER CELLS) here insulin will promote formation of glycogen, triglycerides & proteins

Answer 152

glucose tolerance test if >11.1 = diabetes and <7.8 is normal

Answer 153

insulin deficient insulin cannot be produced in response to high blood glucose level so hyperglycaemia can result no stores of glycogen to break down in low blood glucose hypoglycaemia can occur which can lead to ketoacidosis causes = environmental / genetic

Answer 154

insulin resistant due to elevated insulin levels due to incorrect beta cell response to hyperglycaemia leading to excessive secretion so basal hepatic glucose output will be increased to compensate for lowered blood glucose levels and insulin stimulated muscle glucose uptake reduced due to resistance of insulin links with obesity & inactivity

Answer 155

subcutaneous insulin given basal-bolus (injections before meals) metformin

Answer 156

acute - due to hypoglycaemia chronic - cardiovascular; higher incidence of atherosclerosis & hypertension (which can lead to angina/MI), eye disease; cataracts / maculopathy, diabetic neuropathy; general sensation loss, poor wound healing & increased infection risk

Answer 157

1. food intake may be disrupted 2. poor wound healing 3. increased infection risk

Answer 158

has podocytes which act as basement membrane allows for ultrafiltration which occurs here due to high hydrostatic pressure in kidneys with low osmotic pressure as plasma proteins will oppose filtration; this forces smaller blood constituents out

Answer 159

majority of filtrate will be absorbed, dependent on Na+/K+ pump Na+ moved out of PCT, Cl- follows due to electric gradient produced water reabsorbed via osmotic forces substances that cannot be filtered in glomerulus will be secreted here reabsorption & secretion occurs against concentration gradient so ATP required

Answer 160

concentrates urine & regulated by ADH ascending limb impermeable to water & here using triporter pumps, Na, Cl & K removed this produces concentrated hyperosmolar environment in medulla that causes water to be removed from descending limb whilst urea is added produced counter current multiplier system in which urine is concentrated

Answer 161

blood supply to capillaries

Answer 162

Na, Cl, K regulated here Na & H2O reabsorption with H+ & K+ secretion controlled by aldosterone, AD, ANH

Answer 163

controlled by ADH water reabsorbed here

Answer 164

anti diuretic hormone secreted from posterior pituitary when water is needing to be lost

Answer 165

regulated by RAAS will cause proximal & distal tubules to reabsorb more water & sodium but secrete more potassium

Answer 166

secreted by kidney in response to hypoxia - increases release of RBCs in bone marrow

Answer 167

pre renal - hypoperfusion of kidney (not enough O2; occurs in hypovolaemic shock or renal vascular disease - reduction in blood flow to kidneys due to atheroma in atheroma in aorta / renal artery) renal - problem in kidney itself; glomerulonephritis or 2ndary cause i.e. diabetes, hypertension or drug therapy post renal - renal outflow obstruction i.e. passing kidney stone or tumour compressing urethra

Answer 168

rapid loss over a few days creatine in excess of 200umol/L cause is usually pre renal

Answer 169

occurs over a no of yrs causes = glomerulonephritis / polycystic kidney disease / nephrotic syndrome

Answer 170

NSAIDs - inhibit prostaglandin synthesis which is required for opening & closing of kidney blood vessel valves cyclosporin - nephrotoxic tetracyclines

Answer 171

reduce rate of decline of kidneys by eliminating nephrotoxic drugs & controlling hypertension, diabetes, vasculitis disease if post renal - removal of i.e. gall stones replace function via dialysis only real cure is replacement

Answer 172

1. haemodialysis - outside body, arteriovenous fistula between elbow & wrist placed, heparin also injected as anticoagulant to stop blood clotting in dialyser 2. peritoneal dialysis - inside body in peritoneal sack

Answer 173

peritoneal done in body so no impact but haemodialysis is not so ptx must be treated after session