Week 10

Question 1

Cardiac symptoms/physiology of pregnancy

Answer 1

Increase cardiac output in pregnancy to meet respiratory and metabolic demands of the foetus, oedema because of lower venous return. Varicose veins can occur. Progesterone increases vascular dilation to do this. Cardiac output also increases during labour to increase contractions and provide more oxygen to the baby.

Because of the decreased peripheral resistance, blood pressure shouldn’t rise. Sometimes in second trimester the diastolic bp will decrease.

Flushing, breathlessness, swollen ankles.
Increased renal perfusion means the kidney can’t accommodate the additional filtration load so there is greater urinary frequency. x2 blood flow, smooth muscle relaxes 12-> 75ml, GFR inc 50% and leakage of protein and glucose, urea, creatinine. Osmolality falls by 10mosmoles/kg. Gain 6-8 L water

Plasma volume increases by 50%
HR increases by 15-20 bpm
Cardiac output increases by 40%
Systemic vascular resistance dec
venous return reduced by gravid uterus

Question 2

GI symptoms/physiology of pregnancy

Answer 2

Progesterone causes weight gain. In pregnancy it causes that and relaxation of smooth muscle- lower oesophageal sphincter pressure decreases = reflux. Also a decrease in gastric peristalsis = nausea and constipation.

Reduced metabolic rate of 10-15% and greater insulin resistance. Total weight gain is a round 12.5kg

Can get stretch marks, breast growth, anaemia.

Question 3

Lactation

Answer 3

Colostrum from 16-22nd weeks. Post delivery, milk production is controlled by prolactin in the anterior pituitary gland, and secretion via oxytocin (posterior). The first few days of new-born’s colostrum has high levels of protein and antibodies.

Can get pelvic pain from progesterone, urinary frequency, postpartum depression.

Question 4

Pre eclampsia

Answer 4

Associated with raised bp >160/90 and incr protein. Incr capillary permeability and platelet thrombosis.

Symptoms headache, visual disturbances, epigastric and RUQ pain, nausea and vomiting, rapid oedema.

Can prevent with 300mg aspirin from 12 weeks.

Complications: uncontrolled bp, eclampsia, HELLP, renal failure, hepatic rupture, pulmonary oedema, placental abruption, foetal growth restriction, stillbirth.

Question 5

Tests of renal function

Answer 5

Homeostasis: Na, K, HCO3-, Cl, urine content and volume, osmolality

Glomerular filtration: serum creatinine/urea, creatinine clearance, urine protein/albumin

Endocrine: Vitamin D- PTH and bone profile, erythropoietin- FBC, renin- BP

Question 6

Causes of acute renal failure

Answer 6

Acute tubular necrosis, glomerular diseases, tubo-interstitial disease, vascular diseases, contrast media nephropathy, poisoning.

Question 7

Causes of renal failure or AKI

Answer 7

Prerenal:
sepsis, haemorrhage, hypovolaemia,cardiac failure, hepatorenal syndrome, renovascular insult.

Intrinsic/renal:
Glomerulonephritis/vasculitis, tubulointerstitial nephritis, rhabdomyolysis, myeloma, haemolytic uremic syndrome, malignant hypertension. Usually shows blood or proteinurea.

Post renal:
Calculus, malignancy, prostatic hypertrophy, urethral stricture. All block outflow.

Question 8

Stages of acute kidney injury

Answer 8

1- rise of 26umol/L creatinine or 1.5-1.9 x baseline over 48hrs. + urine < 0.5mL/kg/hr for over 6hrs.

2- 2-2.9x baseline creatinine with urine output <0.5mL/kg/hr for >12hrs

3- 3x baseline creatinine or over 354umol/L with urine output <0.3mL/kg/hr for >24hrs or anuria >12hrs

AKI complications: hyperkalaemia, metabolic acidosis.

Question 9

Other tests in renal failure

Answer 9

albumin (nephrotic syndrome), FBC (anaemia if chronic failure, haemolysis, infection/sepsis), CRP (inflammation or infection), Blood culture (sepsis), coagulation (septicaemia (presepsis)), creatinine kinase (muscle damage or rhabdomyolysis).

Serum protein electrophoresis (myeloma), uric acid (gout), Anti glomerular basement membrane AB-GN

Bone profile of calcium and phosphate-
phosphate is inc in chronic kidney failure, decreased calcium as a result. If calcium is increased, could be multiple myeloma, hyperparathyroidism or malignancy.

Question 10

Endocrine function of the kidneys

Answer 10

erythropoietin production is 80% in the kidney. Released in response to hypoxia, targets bone marrow and important for RBC development.

Renin- enzyme secreted by juxtaglomerular apparatus to convert angiotensinogen to angiotensin 1, for ACE to then turn to angiotensin 2.

Question 11

Protein values of the urine

Answer 11

Normal: <2.5 albumin and <15 protein and <150 mg/24hr

Microalbuminuria is >2.5 men and >3.5 women, <15mg/mmol total, <150 per 24hr.

Proteinurea is dipstick + or ++ with protein 30-350mg/mmol and 300-3500 per 24hr

Nephotic is +++ or >350mg/mmol or >3500 per 24hr

Question 12

Hemlock poisoning

Answer 12

tremor, increased salivation, dilated pupils, muscle pain, initial tachycardia followed by bradycardia, progressive respiratory failure, convulsions, coma and death.

Hemlock is piperidine alkaloid- activates nicotinic receptor.

Question 13

Death cap mushroom poisoning

Answer 13

Delayed onset abdominal pain, diarrhoea and vomiting that settles after a few days. Delayed death from liver failure, kidney failure and DIC, 1-2 weeks after ingestion.

Death cap mushrooms have cyclic peptide amatoxins and phallotoxins that cause liver and kidney failure.

Question 14

Foxglove poisoning

Answer 14

Stomach cramps, blurred and altered colour vision, confusion, bradycardia, hypotension and death.

Cardiac glycosides cause fatal brady and tachyarrhythmias.

Question 15

Aconite

Answer 15

Rapid onset of nausea, vomiting, numbness and burning/tingling, brady and tachyarrhythmias, weakness, paralysis and death.

Aconite has diturpenoid alkaloids that activate cardiac voltage gated sodium channels.

Question 16

How to minimise poison

Answer 16

Activated charcoal has large surface area to weight, it binds to and inactivates a variety of compounds that binds and inactivates substances in the GI tract. Won’t work for iron, lithium, cyanide nor alcohols.

Will work for carbamazepine, phenytoin, salicylate, warfarin, theophylline, verapamil.

There’s also whole-bowel irrigation, urine alkalinisation for salicylates and urine acidification for amphetamines.

Haemodialysis for salicylate, isopropanol, lithium, methanol, ethylene glycol and ethanol.

Intralipid can be used for lipid soluble drugs, eg local anaesthetics, verapamil, chlorpromazine, some tricyclic antidepressants and betablockers.

Question 17

Reversal agents for poisoning

Answer 17

desferrioxamine for iron poisoning, digibind antibodies, ethanol for methanol poisoning, NAC in paracetamol poisoning, isoprenaline for betablockers, naloxone for opiates, sodium bicarbonate for tricyclics.

Question 18

Signs of opiate overdose

Answer 18

Reduced consciousness, hypoventilation, pinpoint pupils, hypoxia, acute pulmonary oedema. Naloxone helps the CVD depression.

Question 19

Signs of benzodiazepine poisoning

Answer 19

Excessive sedation and respiratory depression. Can cause coma and death particularly in the context of mixed ingestion with other CNS depressants like alcohol and opioids.

Question 20

Signs of tricyclic poisoning

Answer 20

Initial tachycardia, drowsiness, nausea and vomiting, urinary retention, confusion, agitation and headache. May progress to hallucinations, seizures and cardiac rhythm disturbances due to cardiac sodium channel blockade. Tachycardia and broad QRS.

If ECG changes are a concern, can give sodium bicarbonate by repeated bolus injection. Correction of acidosis to mild alkalosis reduces binding of the tricyclics to the cardiac sodium channel. Seizures can be treated with benzodiazepines.

Question 21

Typical antipsychotics

Answer 21

Dopamine D2 receptor blockade, positive symptoms, side effects include Extrapyramidal signs, tardive dyskinesia, cardiovascular symptoms. Examples are chlorpromazine, haloperidol, fluphenazine, clopixol.

Question 22

Atypical antipsychotics

Answer 22

2nd gen, serotonin 5HT2 and dopamine D4D3 and some D2 receptor blockade, positive and negative symptoms, metabolic, cvs and a few extrapyramidal side effects. Examples are risperidone, olanzapine, quetiapine, aripiprazole, clozapine.

Olanzapine and diabetes as interacts with pancreas and also gives weight gain.

Question 23

Dopamine theory

Answer 23

Schizophrenia theory- hyperactivity of dopamine receptors in the subcortical and limbic brain regions lead to positive symptoms. Negative symptoms come from hypoactivity of dopamine receptors in the prefrontal cortex.

Question 24

What to do if antipsychotic resistant in schizophrenia?

Answer 24

Give clozapine- not first line though because of agranulocytosis and low neutrophil count- must be monitored regularly. If patient doesnt take clozapine for more than 24hrs have to begin again at their starting dose that might not be so therapeutic.

It has extrapyramidal signs, dystonia muscle contractions acutely (risk tongue obstruction- give anticholinergics), akathisia restlessness, Parkinson’s symptoms within the first few months and tardive dyskinesia after years that could be irreversible.

The dystonias also occur in proclorperazine and metaclopramide.

Question 25

Side effects of lithium for 1st line bipolar

Answer 25

Nephrogenic dm, hypothyroidism, fine tremor, weight gain. is a stabiliser and often given after an antipsychotic like olanzapine.

Lithium toxicity is a complication very long term use and can be triggered when combined with SSRIs and infections. Gives apathy, restlessness then vomiting, diarrhoea, ataxia, weakness, dysarthria, muscle twitching, tremor, confusion. Then in severe poisoning: convulsions, coma, renal failure, electrolyte imbalance, dehydration and hypotension >2mmol/L.

Question 26

Pregabalin

Answer 26

Has street use and is addictive. same with benzodiazepines, which can also worsen anxiety or give withdrawal anxiety. don’t use over two weeks.

Question 27

Acute Tubular Necrosis

Answer 27

Acute tubular necrosis is kidney injury caused by damage to the kidney tubule cells (kidney cells that reabsorb fluid and minerals from urine as it forms).

. The most common causes are

An episode of low blood pressure, leading to insufficient blood flowing through the kidneys
Drugs that damage the kidneys
Serious body wide infection (sepsis)

Question 28

Serotonin syndrome

Answer 28

Spontaneous clonus
Inducible clonus and agitation or diaphoresis
Ocular clonus and agitation or diaphoresis
Tremor and hyperreflexia
Hypertonia
Temperature above 38°C and ocular clonus or inducible clonus
SS is a clinical diagnosis; no laboratory test can confirm the diagnosis. SS can manifest a wide range of clinical symptoms from mild tremor to life-threatening hyperthermia and shock.
Examination findings can include: hyperthermia, agitation, ocular clonus, tremor, akathisia, deep tendon hyperreflexia, inducible or spontaneous clonus, muscle rigidity, dilated pupils, dry mucus membranes, increased bowel sounds, flushed skin, and diaphoresis. Neuromuscular findings are typically more pronounced in the lower extremities.
The following tests may be helpful in severe cases of SS to narrow the differential and to monitor potential complications:
Complete blood count, basic electrolytes, creatinine, and blood urea nitrogen
Creatine phosphokinase, hepatic transaminases, coagulation studies
Blood culture, urinalysis, urine culture
Chest radiograph
Head computed tomography, lumbar puncture
Differential diagnosis
Neuroleptic malignant syndrome
Anticholinergic toxicity
Malignant hyperthermia
Sympathomimetic toxicity
Meningitis or encephalitis
Treatment
Discontinue serotonergic agents
Sedate using benzodiazepines (eg, lorazepam 1 to 2 mg IV per dose; 0.02 to 0.04 mg/kg per dose in children): goal is to eliminate agitation, neuromuscular abnormalities (eg, tremor, clonus), and elevations in heart rate and blood pressure; titrate dose to effect
Provide: oxygen (maintain SpO2 ≥94); IV fluids; continuous cardiac monitoring
Anticipate complications; in severe SS vital signs can fluctuate widely and rapidly
If benzodiazepines and supportive care fail to improve agitation and abnormal vital signs, give cyproheptadine (12 mg orally)
Treat patients with temperature >41.1°C with immediate sedation, paralysis, and endotracheal intubation; treat hyperthermia with standard measures; avoid antipyretics such as acetaminophen

Question 29

Neuroleptic malignant syndrome

Answer 29

Neuroleptics within 1 to 4 weeks.
Hyperthermia (above 38°).
Muscle rigidity.
Five of the following:
Changed mental status.
Tachycardia.
Hypotension or hypertension.
Tremor.
Incontinence.
Diaphoresis (excessive sweating) or sialorrhoea.
Increased creatine phosphokinase (CPK) or urinary myoglobin.
Metabolic acidosis.
Leukocytosis.
Exclusion of other illnesses (neuropsychiatric, drug-induced, systemic).

Airway and breathing need to be protected if there is evidence of compromise. Severe cases may require circulatory and ventilatory support.

Agitated patients require intravenous (IV) benzodiazepines. Physical restraint is best avoided or minimised, as it can worsen the hyperthermia.
The offending drug should be discontinued.
IV fluids should be given for dehydration.
If there has been a recent overdose of the agent then activated charcoal may help to prevent absorption.
Cooling devices and antipyretics are used to treat hyperthermia.
If rhabdomyolysis and acute kidney injury occur then alkalinisation of urine and dialysis are often required.
Dopaminergic drugs, such as bromocriptine and amantadine and muscle relaxants, such as dantrolene sodium, are frequently used in severe cases but there is little empirical evidence for their efficacy. However, there are many anecdotal reports of their usefulness.
Electroconvulsive therapy (ECT) is sometimes used if medication fails to improve the condition and there appears to be some evidence to support its use.

Complications:
Cardiac arrest.
Rhabdomyolysis.
Acute kidney injury.
Seizures.
Respiratory failure.
Disseminated intravascular coagulation.
Aspiration pneumonitis.
Deterioration in psychiatric condition due to drug withdrawal.
Infection.
Hepatic failure.
Pulmonary embolism.

Question 30

Transfusions

Answer 30

45% of UK is O, 40% A, 10% B and 5% AB if Caucasian. Most transfusion reactions are due to antigens and antibodies against other blood types acquired easily from environmental exposure. The antibodies always have an igM component with ten binding sites.

RhD blood mismatch isn’t always very harmful, sometimes it is given on purpose. Rh- blood is hard to find as there are few black donors.

To find a suitable sample match, group and screen is used and coombs reagent to identify the antibodies of this blood type, often now test two samples.

Question 31

Extras about pneumothorax

Answer 31

Smoking gives 10-100 x risk of lung collapse and cannabis much more. Male to female ratio is 5:1. More likely to occur if someone is taller or has apical blebs (likely if there is a connective tissue disorder).

Measure a pneumothorax from intrapleural distance at the level of the hilum. Tap using Salbinger anterior side of anterior axillary line.

Risk of a second pneumothorax much higher than before.

If it is bilateral, fluid effusion is likely to be transudative.

A tension pneumothorax gives CVD symptoms. Every breath traps more air, as pressure rises the heart is under more strain and also can’t perfuse the pressurised lungs and carry oxygen-> cardiac arrest.

Question 32

Tension pneumothorax decompression

Answer 32

Needle 2nd intercostal space, misclavicular line and follow with a chest drain.

Question 33

Who gets tension pneumothorax?

Answer 33

Ventilation patients, trauma, resuscitation patients, lung disease, asthma, COPD, blocked or displaced chest drains, non invasive ventilation, hyperbaric oxygen treatment. Be careful of COPD bullae being heard as pneumothorax then giving one on decompression.

Question 34

Unilateral vs bilateral effusion

Answer 34

Unilateral is usually exudative and full of protein. Bilateral is transudative.

Transudative causes= heart failure, liver failure, kidney fluid overload, low albumin (nephrotic and GI).

Concerns of unilateral is empyema collection of pus.

Parapneumonic effusions are effusions from pneumonia. A simple effusion is straw colour and ph more than 7.2. If less and with fibrin = complicated. If high in pus and fibrin = empyema.

Might treat with pleurodesis or tunnelled chest drain.