Medicine Flashcards
What is pulmonary hypertension?
Mean PAP of >25mmHg at rest or > 30 with exercise
Pulmonary venous hypertension is defined as an elevated PCWP > 18
What causes pulmonary hypertension?
Classified according to the World Symposium on Pulmonary Hypertension
Group 1 -due to causes that lead to structural narrowing of the vessels. idiopathic, drug and toxin induced, due to collagen vascular disease, portal hypertension, HIV, congenital heart disease or schistosomiasis, pulmonary veno-occlusive disease, persistent pulmonary hypertension of the new born
Group 2 - secondary to left-sided heart disease - LVSD, LVDD, valvular diseasr, cardiomyopathies
Group 3 - secondary to lung disease or hypoxaemia - CIOPD, ILD, OSA, chronic altitude exposure, alveolar hypoventilation disorders, developmental lung disease
Group 4 - secondary to chronic VTE
Group 5 - due to multifactorial mechanismshaem disorders e.g. SCA, sarcoid, glycogen storage disorders
What is the pathophysiology of pulmonary hypertension?
There are 3 underlying processes
1. Increased flow:
-Left-to-right shunting
-Back up of flow due to LV dysfunciton or valvular heart disease. Results in vascular smooth muscle remodelling and compensatory hypertenison to drive flow forward
2. Puomonary arterial hypertension
- endothelial dysfunction - results in decreased vasodilator production e.g. NO.
- hypoxic pulmonary vasoconstriction
3. Small pulmonary vessel structural change or destruction. e.f. VTE - causing obstruction and increased resistance to flow
-
What ECG changes might you see in a patient with pulmonary hypertension?
Signs of RVH
- p - pulmonale in II and V1 (RA en largement)
- RAD
- Tall R wave V1 and V2
- RBBB
- RV strain pattern - ST depression and TWI in V1-3 in the inf leads
How is pulmonary hypertension managed in the ICU?
Manage underlying cause
- LTOT for advanced CIOPD - reduces HPVC and i proves RV SV and CO
- NIV - for COPD/OSA
- Pulmonary endarterectomy - for pulmonary veno-occlusive disease
- Anti-coagulation for chronic VTE
Medical therapies include
Diuresis - manage RV failure and volume overload
Vasodilators - improve CO by decreasing RV overload - prostacyclins, endothelin-receptor antagonists, phosphodiesterase inhibitors
What is the mortality rate in patients with severe pulmonary hypertension admitted to GICU?
Requirement for inotropic support may be associated with a mortality of 50%
Describe the pathophysiology of right ventricular failure
- RV tolerates increases in preload easily
- tolerates increases in afterload poorly
- sudden increases in PVR increases RVEDP and increases RV work. The raised RVEDP decreases pulmonary perfusion. The flow profile then begins to look like the LV - i.e happening in diastole
- RV dilates to maintain SV
- crescent shape is lost and the IV septum bulges into LV. LV filling then becomes reduced. This is known an ventricular interdependence
- This results in systemic hypoperfusion and a further decrease in coronary perfusion. Unless the RV is offloaded a vicious cycle ensues leading to circulatory failure and death.
What are the causes of right ventricular failure?
Intrinsic RV failure (normal PVR) - RV infarction, cardiomyopathy.
RV failure with increased PVR - PE, pulmonary hypertension, increased PVR (e.e. hypercapnia, acidosis, norad), LVAD implantation
RV with volume overload - LV failure, L-R intracardiac shunting
What are the signs of RHF?
Peripheral oedema, raised JVP, tender hepatomegaly, pansystolic TR murmur, 3rd HS, loud p2 due to raised PAP. Giant V waves if there’s TR.
What might the ECG show in RHF?
RAD RBBB RV strain pattern - ST depression and TWI in V1-3 S1Q3T3 if PE May be normal
What might the CXR show in patients with RHF?
PA dilatation
Oligaemia of affected lung (Westermark’s sign)
What might the ECHO show in RHF?
Dilated poorly functioning RV TR Hypertrophy Septal bulging RV hypokinesia with apical sparing may suggest PE (McConnell's sign)
How should you manage a patient with RHF?
- optimise fluid status. If PVR is high offload with diuretics
- reduce PVR - oxygen, correct pH and CO2, optimise lung volume (PVR is minimal at FRC), consider pulmonary vasodilators e.g. NO, sildenafil
- improve RV function - modify vent settings to offload the RV - avoid high intrathoracic pressures, limit mean airway pressures
- Maintain CPP (DBP > RVEDP). Low dose vaso has a better PVR profile than norad
- add inotrope if TAPSE < 16mm. Adrenaline raises PVR, dobutamine increases CO and causes pulmonary vasodilatation, PDE3 inhibitors e.g. milrinone causes inodilation
- treat co-existing LVF
What is acute liver failure?
Rare, life-threatening illness
Normally in patients without pre-existing liver disease
What are the 3 key features of acute liver failure?
Jaundice, encephalopathy and coagulopathy
What is the classification of acute liver failure?
The O’Grady classification system categorises ALF based on the interval between onset of jaundice and development of encephalopathy
Hyperacute: < 1 week
Acute: 1-4 weeks
Subacute: 4-12 weeks
What are the causes of acute liver failure?
Infective - Hep A-E, HSV, CMV, VZV, EBV
Drugs - paracetamol, phenytoin, valporate, isoniazid, chemo, ecstasy
Toxins - amanita phalloides mushroom
Malignancy - primary/secondary
Vascular - Budd-Chiari (hepatic vein thrombosis), ischaemic hepatitis (hypotension, hypoperfusion, hypoxia-related)
Pregnancy-related: HELLP syndrome, fatty liver
Metabolic disease: Wilson’s disease
Other: Seronegative hepatitis, autoimmune
In paracetamol toxicity, what are the King’s College criteria for liver transplant in acute liver failure?
ph< 7.3
OR
INR > 6.5 and Cr > 300 and grade 3 or 4 encephalopathy
In non-paracetamol ALF what are the Kings criteria for transplant?
INR > 6.5 Or Any three of -age < 11 or > 40 -non hep A,non-hep B or and idiosyncratic drig reaction -not hyperacute -INR > 3.5 -bili> 300
How does acute liver failure present?
malaise, nausea, jaundice with encephalopathy developing over varying time intervals.
It is associated with high cardiac output and low SVR making septic shock a differential
How is encephalopathy graded?
West Haven criteria
Grade 1 - lack of awareness, anxiety or euphoria, shortened attention span
Grade 2 - lethargy or apathy, disorientation in time, personality change, inappropriate behaviour
Grade 3 - Somnolence to semi-stupor, confusion, gross disorientation, remains responsive to verbal stimuli
Grade 4 - Coma
What are the potential mechanisms of renal failure in acute liver failure?
- ATN (most common) secondary to hypovolaemia, hypotension or hypoperfusion, or nephrotoxins e.g. paracetamol
- Secondary to underlying disease e.g. glomerulonephritis in hep b and c
- Intra-abdominal hypertension due to ascites
- Hepatorenal syndrome
What is the ICU management of acute liver failure?
Early referral to a tertiary centre
- I+V for reduced GCS. Avoid high PEEP if possible to avoid increasing hepatic portal venous pressure and ICP
- CV - targeted fluid resus aiming to avoid worsening cerebral oedema, vasopressor to maintain MAP 60-65 and CPP 60-80
- Neuro - head elevation, sedate, avoid hypotension, avoid hypoxia and hypercapnia, avoid fever, normal BM. Mannitol or hypertonic saline for intracranial hypertension
- Renal - may need RRT to avoid fluid overload and acidosis
- Coagulation - product replacement in active bleeding, but not routinely.
What is the mechanism of liver injury in paracetamol overdose?
The metabolite N-acetyl-p-benzoquinone imine (NAPQI) causes the hepatotoxicity.
Normally paracetamol is metabolised by glucoronidation and sulphation. A small amount is metabolised to NAPQI which is then detoxified by glutathione.
In paracetamol OD more is shunted down this route as the glucuronidation and sulphation become saturated, glutathione becomes depleted and the NAPQI builds up causing widespread hepatocyte damage.
What increases your risk for hepatotoxicity following paracetamol OD?
Cytochrome enzyme induction - chronic ETOH, enzyme inducing drugs e.g. carbamazepine, barbituates, rifampicin, isoniazid, st johns wort
2. Glutathione depletion - malnutrition, anorexia, existing liver injury
How is paracetamol OD treated and why?
N-acetylcysteine is a precursor for glutathione
Should be administered within 8 hours
What are the causes of cirrhosis?
Toxins - alcohol
Infective - hep b and c
Drugs - methotrexate, amiodarone
Cholestatic conditions - PBC, PSC
Autoimmune - autoimmune hepatitis
Hereditary - wilsons disease, haemochromatosis, alpha-1 antitrypsin deficiency, type IV glycogen storage disease
Vascular - Budd-Chiari syndrome, veno-occlusive disease
Other - non-alcoholic fatty liver disease
What scoring systems predict mortality in cirrhosis?
Child Pugh
Meld
Describe the Child Pugh scoring system
Encehalopathy Ascites Bilirubin Albumin INR Number of points correlates with a 1 year and 5 year % survival
Describe MELD
Predicts mortality in hospitalised patients
Calculation based on bilirubin, INR and Cr
Why do patients with cirrhosis get admitted to ICU?
Variceal bleeding Encephalopathy Alcoholic hepatitis AKI Severe sepsis
What is the in hospital mortality for patients with cirrhosis?
> 50%
65-90% in those with severe sepsis requiring organ support
What is portal hypertension?
Portal pressure > 10%
A/w development of a porto-systemic collateral venous circulation, ascites and splenomegaly
Diagnosed clinically
How is variceal bleeding managed?
Volume resuscitation Vasoconstrictors e.g. terlipressin OGD and band ligation Antibiotics Sengstaken-Blakemore tube if there is failure to control bleeding until repeat OGD or TIPPS
What is TIPPS?
Transjugular intrahepatic portosystemic stent shunt.
Endovascular procedure that establishes communication between the inflow portal vein and the outflow hepatic vein, using a stemt
Reduces portal pressures in patients with complications due to portal hypertension e.g. variceal bleeding and diuretic refractory ascites
What is hepatorenal syndrome?
Renal failure affecting patients with cirrhosis or fulminant liver failure
It is a pre-renal AKI that is unresponsive to fluid therapy
There is abnormal autoregulation with renal vasoconstriction and dilation of splanchnic vessels
What are the diagnostic criteria for hepatorenal syndrome?
- Cirrhosis with ascites
- Cr > 133
- No improvement in Cr after 2 days of diuretic withdrawal and volume expansion with albumin
- Absence of shock
- Absence of nephrotoxins
- Absence of renal parenchymal disease
What are the types of hepatorenal syndrome?
Type 1 - rapidly progressive decline in renal function, carrying a mortality > 50%
Type 2 - More indolent, a/w diuretic resistant ascites
A trial of treatment with terlipressin and plasma expansion with albumin should be considered. TIPSS will improve renal function. Definitive treatment is with transplant
What is SBP?
Ascitic fluid infection
Normally occurs in patients with cirrhosis and ascites
How might SBP present?
Fever
Hypotension
Abdo pain
Altered mental status
What are the features of hepatopulmonary syndrome?
Intrapulmonary shunting and hypoxia in patients with cirrhosis
Dyspnoea and hypoxia are worse in the upright position
Carries a poor prognosis and is an indication for orthotopic liver transplant in suitable candidates
What are the causes of chest pain?
- Myocardial ischaemia
- Pleuritic chest pain - pneumonia, PE, musculoskeletal
- Aortic dissection
- Pericarditis
5, Gastro-oesophaeal - GORD, dyspepsia
What differentiates MI from angina?
Pain > 20 mins not relieved by nitrates
More likely MI if a/w sweating/nausea/vomiting
Severity - worst pain ever, feeling of impending doom
Describe the pain a/w aortic dissection
Very sudden onset and severe at outset
May have a tearing quality
Often startes in the anterior chest, spreads to neck and then the back over a few minutes
Can start as neck pain - if originating in the arch
Or interscapular pain in those of the descending aorta
What causes pleurisy?
Pneumonia
PE
Pneumothorax
Describe pericardial pain
Worse on inspiration, central, positional ion nature, typically relieved on sitting up.
What are the causes of oedema?
Bilateral - CCF Hepatic failure Renal failure Nephrotic syndrome Malnutrition Immobility Drugs e.g. NSAIDS, calcium channel blockers Unilateral -lymphatic obstruction -venous obstruction e.g. DVT -cellulitis -localised immobility - ruptured bakers cyst
Describe Virchow’s triad
3 factors necessary for the formation of a thrombus
- statis/turbulence of blood flow
- injury to endothelium
-alterations in coagulability
VTE pften occurs in areas of vascular trauma e.g. in response to indwelling devices, or in regions of poor flow
What are the risk factors for VTE?
Venous statis - immobility, long travel, varicose veins
Endothelial injury - indwelling devices, surgery, trauma, burns
Hypercoagulability - malignancy, pregnancy and puerperium, obesity, past hx VTE, drugs e.g. COC, HRT, chemo, smoking, ageing, thrombophilia e.g. factor V leiden, activated protein c resistance, antiphospholipid syndrome, antithrombin and protein c and s deficiencies
How are PEs classified?
- Massive - where theres BP < 90 for at least 15 mins or requiring inotropic support, pulseless, profound bradycardia
- Submassive - PE with RV dysfunction or myocardial necrosis
What might an ECHO show in acute PE?
RV overload and dysfunction
McConnell’s sign - reduced RV free wall contracility with sparing of the apex
What guidelines are there to aid management of PE?
The European Society of Cardiology 2014
Describe the ESC guidelines on the diagnosis of PE
Is CTPA immediately available - if yes proceed to this
If not then ECHO
If there is no RV dysfuction then unlikely PE
If there is RV dysfuction and CTPA unavailable or patient unstable then treat as PE.
How are PEs treated?
- Anticoag - UFH is preferred initial mode
- Thrombolysis - is first line reperfusion therapy, surgical embolectomy may be needed in those with CI to systemic thrombolysis or where thrombolysis has failed to improve the haemodynamic status.
Is there any evidence to support thrombolysis in PE treatment?
The PEITHO trial was an RCT comparing IV tenecteplase plus heparin with just heparin. Patients needed to have evidence of RV dysfunction
There was improved all cause mortality at 7 days, although there were significantly more major bleeding complications in the thrombolysis group including intracerebral.
How can VTE be prevented?
- General measures - mobilise and hydrate
- Non-pharmacological - TEDS, ICDs
- Pharmacological - UFH, LMWH, NOACs
What is heparin?
A large polysaccharide
Naturally occurring anticoagulant
Exerts its effects by binding to endogenous an antithrombin III. This then inhibits factor Xa and IIa
Cleared by the reticuloendothelial system
Describe LMWH
Short chain polysaccharides Work in a similar way to UFH They have a lower risk of bleeding and Complications such as HIT than UFH. Renally excreted No monitoring is required
What is protamine?
Reverses UFH
1mg neutralises 100units of UFH
Give slowly to avoid pulmonary hypertension
May partially revers LMWH but its effects are inconsistent
What causes isolated APTT rise?
Haemophilia A - (factor VIII deficiency) Haemophilia B (Factor IX deficiency) Factor XI deficiency Factor XII deficiency Heparin Antiphospholipid syndrome Artifact
What are the contraindications to heparin?
Allergy
Previous HIT
Active major bleeding or risk of serious bleeding
Platelets < 50
Coagulopathy
Recent neuraxial blockade - don’t do within 12 hours of UFH admin, can be given 4 hours after uncomplicated neuraxial blockade.
What is HIT?
Heparin-induced thrombocytopenia
- Type 1: non-immune mediated, more common, occurs within 3 days of treatment, platelet count 100-150, no bleeding or thrombosis complication, resolves spontaneously
- Type 2: Immune mediated, IgG to heparin/platelet factor 4 complex causes platelet activation and results in arterial and venous thrombosis, 0/6% of patients treated with heparin, more common with UFH, 5-10 days after starting treatment, platelets fall to ~ 50 or by 50%, thrombosis occurs in 20-50%, skin necrosis in up to 20%
How do we diagnose HIT?
-Calculate a pre-test probability
-On the basis of this carry out a test after consulting haematologist
Pre-test probabilty is based on fall in platelets, timing, thrombosis and potential other causes. (the 4T’s)
How is HIT managed?
It’s a prothombotic state
Heparin should be stopped
Alternative anticoag should be started
-Argatoban is the first line choice - it’s a direct thrombin inhibitor and only licensed for use in HIT
-or dabigatran, danaparoid, fondaparinux
-Avoid giving platelets
-warfarin worsens skin necrosis and should be given until plateletns are > 150
-Avoid further heparin for 100 days. No IgM antibodies are produced so the body doesn;t have immunological memory
What is the aetiology of valvular lesions?
- Congential e.g. adult survivors of CHD, or bicuspid aortic valve which predisposes to early calcific aortic stenosis
- Rheumatic fever- causes scarring, thickening and calcification of valves. Mitral > aortic. Rare in developed countries
- Degenerative - acquired calcific aortic stenosis in elderly
- Infective - endocarditis causing destruction of leaflets and chordal rupture
- Prosthetic - artificial valves may degenerate or leak as a result of valve dysfunction or dihiscence or surgical sutures
What is encephalitis?
Inflammation of the brain paraenchyma - normally caused by viruses gaining access to the CNS via haematogenous spread
What are the symptoms of encephalitis?
Personality change Headaches Confusion Seizures including status Focal neurology Coma
What are the caused of encephalitis
Viruses - HSV-1, enterovirus, VZV, EBV, Rabies, CMV
Bacteria, fungi and TB
It can also occur secondary to an nautoimmune process e.g. anti-NMDA receptor or anti-gamma-aminobutyric acid (GABA)-B receptor encephalitis
How is encephalitis diagnosed?
History and exam
Bloods - FBC,(WCC may help differentiate from bacterial meningitis)
- CRP,
- U+Es, LFTs, TFTs (other causes of confusion)
- coag (may have DIC, may need LP)
- blood cultures
- autoimmune serology
-consider HIV
Imaging - CT brain, MRI
EEG
LP - if not contraindicated - cell count and Gram stain, cytology, viral PCR, biochem, culture, autoantibiodies
What are the differential diagnoses of encephalitis?
- Infection - meningitis, cerebral abscess, sepsis, HIV
- Vascular - CVA/TIA, intracranial haemorrhiage, posterior reversible encephalopathy syndrome (PRES)
- Malignancy - primary incl lymphoma, metastases
- Toxin/metabolic encephalopathy - hepatic encephalopathy, uraemia, thyroid crisis, electrolyte disturbance, illicit drugs e.g. cocaine, MDMA, LSD, overdose, seritonin syndrome
- Autoimmune - anti-NMDA or anti-GABA-B receptor encephalitis, vasculitis, cerebral lupus, acute disseminated encephaomyelitis (ADEM) e.g. secondary to viral infection or post rabies vaccine
- Other - non-convulsive status epilepticus
How is encephalitis treated?
ABCDE
Aciclovir 1-mg/kg tds for 14 days
3rd gen cephalosporin to cover bacterial meningitis may be needed
What is the prognosis of encephalitis?
If untreated 80% mortality
If treated 10% mortality
Complication rate is high with memory loss, behavioural and personality changes, speech problems or epilepsy
What are the LP findings in bacterial meningitis?
Opening pressure - high Turbid CSF:plasma glucose low (<50%) Protein (g/l) high >1 Cell count > 1000 per mm3 WCC differential - poly morphs
What are the LP findings in viral meningitis/encephalitis?
Opening pressure normal/high Appearance - gin clear CSF:plasma glucose normal Protein normal Cell count < 500 WCC differential lymphocytes
What are the LP findings in fungal meningitis/encephalitis?
Opening pressure - very high Appearance - fibrin web CSF:plasma glucose - low/normal Protein - high (0.2-5) Cell count 100-500 WCC differential lymphocytes
What are the causes of acute shortness of breath at rest?
Cardiovascular - LVF, acute PE, mitral stenosis
Respiratory - acute severe asthma, exac COPD, pneumonia, pneumothorax, ARDS, anaphylaxis, inhaled foreign body
Other - psychogenic hyperventilation, fever, metabolic acidosis, neurological disease
What are the causes of chronic breathlessness on effort?
CV - chronic heart failure, angina, chronic PE
Resp - COPD, pleural effusion, interstitial lung disease, bronchial cancer, lymphangitis carcinomatosis
Other - physical deconditioning, obesity, anaemia, neurological disease
What are the causes of cough?
Upper resp - URTI, rhinosinusitis, smoking, drugs
Lung disease - Ca, COPD, bronchiectasis, parenchymal lung disease, asthma, bronchitis, foreign body
Cardiac - LVF
Oesphagus - reflux
What are the causes of haemoptysis?
Common - bronchitis, pnuemonia, Ca, bronchiectasis, PE, LVF
Less common - bronchial ademona, mycetoma, vascular malformations, bleeding diasthesis, vasculitis (Wegeners, Goodpastures), connective tissue disease, endometriosis, spurious e.g. nose bleed
What causes wheeze?
Asthma COPD Bronchiectasis Large airway obstruction Pulmonary oedema
What does a polyphonic wheeze indicate?
Multiple simultaneous different pitched sounds occurring during expiration.
Caused by COPD and asthma
What does a fixed monophonic wheeze indicate?
Localised narrowing of a single airway
Might indicate bronchial carcioma
What do respiratory ‘squarks’ mean?
Opening of previously collapsed airway
Typical of extrinsic allergic alveolitis
What protein level in a pleural effusion indicates transudate vs exudate?
Protein < 30 g/dL - transudate
> 30 (or pleural serum protein raito 0.5) indicates exudate
What pH of a pleural effusion would be consistent with empyema?
pH < 7.2
What are the common causes of a transudative pleural effusion?
Cardiac failure
Nephrotic syndrome
Hepatic cirrhosis
Hypoalbuminaemia (malnutrition, chronic disease, malabsrption)
What are the uncommon causes of transudative pleural effusions?
Pericardial constriction
Meig’s syndrome (Ovarian fibroma)
Myxoedema
What are the common causes of exudative pleural effusion?
Bacterial pneumonia
Carcinoma
Mesothelioma
What are the less common causes of exudative pleural effusion?
TB Haemothorax Pancreatitis Sub-phrenic abscess Autoimmune disease Chylothorax Yellow nail syndrome (abnormal lymph drainage leading to yellow nails, pleural effusion and lymphoedema)
How should pleural effusions be investigated?
CXR Confirm pleural effusion may require USS Aspirate - LDH, pH, cytology CT thorax Pleural biopsy TFTs, u+es, LFTs, albumin ECHO
What LDH level is consistent with a pleural effusion being a transudate vs an exudate?
LDH < 200u = transudate
LDH > 200u (or pleural/serum ratio > 0.6) = exudate
What are the causes of pnuemothoraces?
Primary - implies normal lung and due to a ruptured pleural bleb
Secondary - occurs in association with underlying lung disease. Rupture of the visceral pleura results in communication between airway and pleural space
Traumatic
What is a closed pneumothorax?
The leak closes as the lung deflates so the amount of air escaping into the pleural space in limited, pleural pressure remains negative and resolution occurs slowly even without treatment
What is an open pneumothorax?
Occurs when persistent communication between the airway and the pleura develops (bronchopleural fistula), which is seen as a persistent bubbling of the chest drain
-The lung cannot re-expand and there is significant risk of infection being transmitted from the airway
How is a pneumothorax managed?
Small pnemothoraces in asymptomatic patients may required no treatment
Trial of aspiration is appropriate larger pneumothoraces and where patients are symptomatic - if unsuccessful ICD will be needed.
Surgical treatment may be required if non-resolving e.g. pleural abrasion or pleurectomy
Should not travel on an aeroplane for 3 months.
What is diarrhoea?
According to the WHO it’s the passage of 3 or more loose or liquid stools per day
Of type 6 or 7 stool as per the Bristol Stool Chart
What is the incidence of diarrhoea in ITU?
25-50%
What is the pathophysiology of diarrhoea?
Imbalance of water and solute transport in the GIT resulting from osmosis, secretion, inflammation or dysmotility
What are the causes of diarrhoea in ITU?
Infective causes
- bacterial e.g. e.coli, salmonella, campylobacter jejuni, clostridium difficile, Shigella
- viral e.g. noravirus, rotavirus
- fungal e.g. candida
- protozoal e.g. cryptosporidia, giardia lamblia
Non-infective
- IBD
- Drug related e.g. NG feed, antibiotics, oral magnesium, laxatives, chemo, alcohol, antacids
- mesenteric ischaemia
- bacterial overgrowth
- short gut syndrome
- post ileus recovery or overflow diarrhoea
- food intolerance
- others e.g. anxiety, IBS
What is osmotic diarrhoea?
Failure of the GIT to absorb osmotically active solutes - meaning that water is retained within the gut lumen e.g. NG feed associated diarrhoea
What is secretory diarrhoea?
Increased secretion or reduced absorption of salt and water across the gut mucosa, often results in large volume diarrhoea, doesn’t improve with starvation.
e.g. enterotoxin production e.g. Vibrio cholerae and laxatives
What is inflammatory diarrhoea?
Loff of integrity of the GI mucosa due to inflammation resulting in impaired absorption of bowel contents and exudative fluid loss
Bloody diarrhoea may result if it affects the large bowel
e.g. IBD
What is dysmotility diarrhoes?
Rapid transit time throught the GIT and the water and electrolytes from the small bowel overwhelm the absorptive capacity of the colon
e.g. post ileus.
