Explain That Condition Flashcards
Explain: Anaphylaxis
the Australasian Society of Clinical Immunology and Allergy describes it as:
- Anyacute onset illnesswithtypical skin features(urticarial rash or erythema/flushing, and/or angioedema),PLUSinvolvement ofrespiratoryand/orcardiovascularand/or persistent severegastrointestinalsymptoms.
OR
- Anyacute onsetofhypotensionorbronchospasmorupper airway obstructionwhere anaphylaxis is considered possible, even if typical skin features are not present.
It is a term used to describe a rapid and generalised hypersensitivity after exposure to an antigen. It differs from a simple allergic reaction in that it has systemic effects.
Define: Orthostatic hypotension
A drop in blood pressure when standing, due to sluggish or inactive baroreflexes.
Presents with blurred vision and dizziness.
Define: dissecting aneurysm
Accumulation of blood between the tunica layers of the vessels. A tear in the tunica causes rupture of the vasa vasorum.
Define: pulmonary contusion
Direct bruise of the lungs, which causes alveolar haemorrhage and oedema. Key signs: Dyspnea Hypoxia Tachypnea Hemoptysis
Explain: postprandial hypotension
A drop in blood pressure after eating a meal. Caused by blood flow being redirected to the digestive system. More common in older adults. Associated with lightheartedness and syncope.
Explain: osmotic diuresis
Too many non-absorbable substances in the blood.
Filtered out by the kidneys and flushed out with water in the body, increasing urine output.
Increase urine output, bladder discomfort, thirst, poor sleep (always gotta pee), fatigue (loss of nutrients and salts), elevated calcium levels in the blood, possible heart failure.
Explain: type 1 diabetes mellitus
Absolute deficiency.
An autoimmune condition in which the immune system is activated to destroy the beta cells in the pancreas, which produce insulin.
Early onset (11-13 years), impacts growth.
Insulin promotes breakdown of glycogen stores - blood sugars increase because no insulin to activate receptors for uptake.
Inability to transport fuel substrates in to cells.
Manifestation/ presentation:
Initially presents with a 1-4 week illness. Plasma glucose exceeds renal threshold for glucose reabsorbtion, leading to glucose excretion in urine (glycosuria), causing osmotic effect, leading to cellular dehydration and hypovolemia.
Management:
Insulin replacement organised and modified with GP.
Fast: clear, onset 1-20 mins, peak 1 hr, duration 3-5 hrs.
Short: onset <30 mins, peak 2-4 hrs, duration 6-8 hrs.
Intermediate: cloudy, onset 1-1.5 hrs, duration 4-12 hrs.
Mixed: combination.
Explain: type 2 diabetes mellitus
Impaired insulin secretion (<50%) or impaired action (cell response).
Risk factors: obesity, inactivity, age, low birth weight, maternal history.
Manifestation: gradual and insidious onset. Polyuria and nocturia. Thirst, blurred vision (not every pt).
Management: diet and exercise, oral antihyperglycaemics e.g. metformin, diamicron, daonil, thiazolidinediones, insulin.
We can advise pts to make lifestyle changes.
Explain: gestational diabetes
3-8% of pregnant women develop in 24-28th week of pregnancy.
Risk factors: >30 years, family hx DMT2, overweight, ATSI, Asian and hx of GD.
Insulin resistance and inadequate insulin secretion.
Women revert back after birth.
High incidence of repeat in further pregnancies.
Explain: diabetic ketoacidosis
Metabolic acidosis - ketone bodies.
Mortality 3-5%.
Characterised by hypoglycaemia, metabolic acidosis and hyperketonaemia.
Deficiency of insulin —> hyperglycaemia —> body breaks down proteins for energy —> anaerobic fuel —> produces ketones —> blood pH becomes more acidic.
Hyperglycaemia leads to osmotic diuresis, dehydration, electrolyte loss.
Hyperketonaemia causes increased synthesis of ketone bodies from fatty acids.
Clinical manifestations:
Polyuria, polydipsia, polyphagia.
Nausea and vomiting.
Cramps, malaise.
Kussmaul respiration (sweet smell on the breath).
ALOC.
Possible recent illness or infection.
Considered a medical emergency, even if they appear well.
Management:
IV rehydration: only 20-40% of IV crystaloids remain in bloodstream, rest is excreted —> young, fit and healthy individuals can take a lot of fluids and not go in to heart failure.
Insulin: pt may have a ‘rescue plan’ —> let them go through with it, if it fits.
Electrolyte imbalance: requires measuring blood gases at hospital —> transport.
Explain: hypoglycaemia presentation
Symptoms are usually the result of either reduced glucose to the brain or the release of adrenaline.
<3mmol/L non-diabetic, <3.5mmol/L in diabetics.
Decreased glucose: Decreased LOC Confusion Headache Drowsiness Disorientation Unresponsiveness Seizure Stroke
Release of adrenaline: Diaphoresis Tremors Weakness Hunger Tachycardia Dizziness Pale, cool, clammy skin Warm sensation
Explain: digoxin toxicity
Digoxin toxicity is characterised by gastrointestinal distress, hyperkalemia and life-threatening dysryhthmias, including increased automaticity and AV nodal blockade
Digoxin has a narrow therapeutic index and chronic toxicity is more likely in the elderly and those with renal impairment.
Can be acute or chronic.
Acute digoxin toxicity clinical features:
Time course: initial toxic effects of nausea and vomiting occur at 2-4 hours, peak serum levels at 6 hours and life-threatening cardiovascular complications at 8-12h
GI: anorexia, nausea, vomiting, diarrhoea, abdominal pain
METABOLIC: hyperkalaemia (early sign of significant toxicity)
CVS: enhanced automaticity (atrial tachycardia (e.g. flutter, AF) with AV block, VF, VT, ventricular ectopic beats), bradyarrhythmias (Conduction delays / blocks, slow or regularised AF), hypotension, shock
CNS: lethargy, confusion
Explain: thyroid storm
Rare form of hyperthyroidism.
During thyroid storm, an individual’s heart rate, blood pressure, and body temperature can soar to dangerously high levels.
Thyroid storm, also referred to as thyrotoxic crisis, is an acute, life-threatening, hypermetabolic state induced by excessive release of thyroid hormones (THs) in individuals with thyrotoxicosis. Thyroid storm may be the initial presentation of thyrotoxicosis in undiagnosed children, particularly in neonates.
Explain: acute bronchitis
Inflammation of the lining of bronchial tubes, which carry air to and from the lungs.
Acute bronchitis is often caused by a viral respiratory infection and improves by itself.
Explain: bronchiolitis
Hey hx/assessments: A - allergies M – medications P – past medical history (birth gestation and weight, immunisation status, antenatal problems, mode of delivery, neonatal ventilation, other syndromes: trisomy 21) L – last feed E – events:
how did illness start? -> presentation before day 3 is more severe.
illness starts as a coryzal illness -> peak of respiratory distress @ 3 days and then settles over 7-10 days.
URTI
apnoea
blue spells
ability to feed
respiratory function
possible evidence of secondary bacterial infection (streptococcus or staphylococcus)
EXAMINATION
general: temperature, P,
respiratory: RR, WOB, grunting, nasal flaring, indrawing, retraction, apnoeas
cardiovascular: perfusion, murmurs, pulses, heart failure
