Explain That Condition Flashcards
(33 cards)
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
Explain: disseminated intravascular coagulopathy
AKA: DIC, consumptive coagulopathy.
A condition affecting the blood’s ability to clot and stop bleeding.
In disseminated intravascular coagulation, abnormal clumps of thickened blood (clots) form inside blood vessels. These abnormal clots use up the blood’s clotting factors, which can lead to massive bleeding in other places. Causes include inflammation, infection and cancer.
Explain: Ebola
Humans are not infectious until they develop symptoms, then the virus is infectious through blood and body fluids. Sudden onset: Fever and fatigue Myalgia Headache Sore throat Later onset: Rash D and v Internal/external bleeding Liver and kidney impairment
Explain: headache
Pathology:
Overall brain tissue has limited sensitivity to pain.
Structures capable of producing pain: skin, major cranial vessels, dura, nerves, muscles.
Muscle contraction - tension headache.
Stretching of intracranial pressure - tumor, trauma.
Dilation of vascular structures - throbbing, usually migraines —> vasoconstriction followed by vasodilation (rebound effect); meds vasoconstrict.
Inflammation - meningitis, sinusitis, ear ache, tooth ache.
Explain: migraine
19th most common disease, more common in women.
“Headache plus” syndrome (other symptoms) —> pristine, aura (1 in 3), nausea and vomiting, photophobia, phonophobia.
Genetic predisposition.
Tension type:
Bilateral, non-pulsatile and mild/moderate headache.
If migraine caught early enough, paracetamol, ibuprofen and it’s of water may abate it.
Explain: cluster headache
Thought to be caused by dysfunction of CNV.
Acute onset, severe in nature, unilateral, periorbital, temporal pain.
Associated factors: lacrimation, eyelid ptosis, facial swelling.
Alarm clock - tend to occur in clusters, daily, same side of face, for several weeks. Can mimic stroke symptoms.
More common in men.
Explain: UTI
Inflammation of the urinary epithelium.
Can occur anywhere along the tract.
Bacterial infection occurs through retrograde movement of bacilli into urethra and bladder.
More common: women, uncircumcised men, catheter insitu, unprotected sex, pregnancy, elderly.
Presentation - elderly may feel less pain, experience confusion and odorous urine.
Management- elderly require transport for complex management, young can visit a GP.
Explain: nephrolithiasis
Kidney stones.
More common in men.
Classified according to primary minerals - calcium (alkaline urine) (70-80%), magnesium, uric acid.
Risk factors: age 20-30, family hx, gender, fluid intake (dehydration), geographic location, urine pH.
Presentation- asymptomatic while not lodged anywhere.
Sever pain in lumbar-inguinal region (the back—> toward the groin; renal —> ureteral).
Haematuria (May/may not be frank).
Rigours accompanied with fever.
Renal colic: entered ureter.
Management:
Breakthrough meds to help them move.
IV fentanyl.
Methoxyflurane (note: has renal implications, cancer)
Morphine (longer acting).
IV fluids: create more filtrate —> open up lumen —> allow stone to pass (may still need lasering).
Antiemetic (not prophylactically with opioids).
Explain: pylonephritis
Infection of the renal pelvis, medulla and cortex.
Ascending movement of micro-organisms along urinary tract (e coli causative).
Infiltration WBC, oedema, purulent urine.
More common in women.
Presentation:
Dysuria
Frequency
Hesitation
Dark, odorous urine
ALOC in prolonged cases
Management:
Urinalysis, urine culture, antibiotic therapy.
Explain: glomerulonephritis
Inflammation of the glomerulus brought on by immune disorders —> 7-14 days after strep infection, scarlet fever etc. —> results in changes in membrane permeability.
Abrupt onset: symptoms obscure 10-21 days post infection.
Most common cause of chronic kidney disease.
Presentation:
Haematuria and proteinuria
Decreased GFR and oliguria
Hypertension
Peripheral oedema: puffy ankles and feet because fluid has to leave vascular space.
Management:
Caution- don’t give fluids
Antibiotic (treating primary cause), managing hypertension and oedema, steroids to suppress inflammatory responses.
