Medicine Flashcards
Grading scale for murmurs
Levine scale
1 slightest possible murmur heard by trained ear
2 soft murmur heard when in optimal condition
3 moderately loud. no thrill
4 loud and associated with a palpable thrill
5 loud with thrill. heard with stethoscope lightly touching chest
6 loud, thrill heard with stethoscope not touching skin
Guilliain- Barre syndrome is most likely associated with which organism
Campylobacter jejune
Guilliain-barre symptoms are caused by..
loss of myelin
GBS definition
acute rapidly evolving demyelinating inflammatory polyradiculoneuropathy that often starts
in the distal lower limbs and ascends
signs and symptoms of GBS
■ sensory: distal and symmetric paresthesias, loss of proprioception and vibration sense, neuropathic
pain
■ motor: weakness starting distally in legs, areflexia
■ autonomic: blood pressure dysregulation, arrhythmias, bladder dysfunction
investigation for GBS
■ CSF: albuminocytologic dissociation (high protein, normal WBC)
■ EMG/NCS: conduction block, differential or focal (motor > sensory) slowing, decreased F-wave,
sural sparing
subtypes of GBS
• subtypes
- acute inflammatory demyelinating polyneuropathy (AIDP)
- acute motor-sensory axonal neuropathy (AMSAN)
- acute motor axonal neuropathy (AMAN)
treatments of GBS
• treatment
■ IVIG or plasmapheresis, ± pain management, monitor vitals and vital capacity
antidote for nerve gas poisoning
atropine
Diabetic retinopathy - clinical features
Non proliferative
pre proliferative
proliferative
leading cause of blindness
diabetic retinopathy
prevention of diabetic retinopathy
Tight glycemic control
Annual visits to optometrist or ophthalmologist
what is diabetic retinopathy
a microvascular complication of poorly controlled diabetes.
treatment of diabetic retinopathy
Pan-retinal and focal retinal laser
photocoagulation reduces the risk of visual loss
in patients with macular edema.
intravitreal injection of corticosteroid or anti-VEGF for foveal involved diabetic macular edema
how does loss of vision occur in diabetic retinopathy
loss of vision due to
■ progressive microangiopathy leading to macular edema
■ progressive DR → neovascularization → traction → RD and vitreous hemorrhage
■ rubeosis iridis (neovascularization of the iris) leading to neovascular glaucoma (poor prognosis)
■ macular ischemia
non- proliferative diabetic retinopathy
increased vascular permeability and retinal ischemia
■ microaneurysms
■ dot and blot hemorrhages
■ hard exudates (lipid deposits), non-specific for DR
■ macular edema
pre-proliferative diabetic retinopathy
■ non-proliferative findings plus:
◆ venous beading (in ≥2 of 4 retinal quadrants)
◆ intraretinal microvascular anomalies (IRMA) in 1 of 4 retinal quadrants
– IRMA: dilated, leaky vessels within the retina
◆ cotton wool spots (nerve fibre layer infarcts)
proliferative diabetic retinopathy
■ 5% of patients with DM will reach this stage
■ neovascularization of iris, disc, retina to vitreous
◆ neovascularization of iris (rubeosis iridis) can lead to neovascular glaucoma
◆ vitreous hemorrhage, bleeding from fragile new vessels, fibrous tissue can contract causing
tractional RD
■ high risk of severe vision loss secondary to vitreous hemorrhage, RD
soft exudates indicate ischaemia
extra ocular muscle palsy associated with diabetic retinopathy
- usually CN III infarct
- pupil usually spared in diabetic CN III palsy, but ptosis is observed
- may involve CN IV and VI
- usually recover within few months
peripheral neuropathy facts
- as proprioception reduces it becomes more difficult to walk on uneven surfaces
- many patients are injured yearly by putting their feet on radiators or sitting to close to the fire.
- specific footwear to protect feet
- foot shape changes due to glycosylation of collagen
- charcot Joint
microvascular complications of diabetes
Neuropathy, retinopathy, nephropathy, glaucoma and cataracts
microvascular complications of diabetes
coronary artery disease, Stroke, peripheral vascular disease (and therefore ulcers and gangrene)
other complications of diabetes
increased risk of infections pregnancy complications metabolic difficulties impotence autonomic neuropathy
causes of sudden loss of vision in diabetic patients
central retinal artery occlusion
retinal detachment
vitreous haemorrhage
eye assessments for diabetic patients include
opthalmoscopy through dilated pupils
retinal photography
fluorecein angiography
slit lamp examination
what is peripheral neuropathy
a symmetrical sensory polyneuropathy, initially affecting distal lower extremities.
decreased or loss of ankle reflexes occurs early in disease.
progressive loss increases the risk of ulcer formation
large fibre loss - peripheral neuropathy
loss of vibration
loss of proprioception
Small fiber loss peripheral neuropathy
loss of light touch
loss of temperature
impairment of pain
drugs approved by Health Canada for peripheral neuropathy
duloxetine
pregabalin
Dengue fever
Common Arboviral infection
clinical incubation period dengue fever
5-10 days
vector for dengue fever including breeding areas
Aedes aegypti mosquito which prefers to breed in clean water and common in urban areas with higher incidences in the Welter months
symptoms of dengue fever
lethargy
biphasic fever (present for 2 days which resolves and is then followed by a second fever)
headache - especially retro orbital pain
arthralgia
myalgia
rash - usually with second fever. maculopapular starting on trunk and spreading to limbs
Severe cases/complications of Dengue
Dengue shock syndrome
Dengue haemorrhage fever
these have immunological basis - if previous immunity to dengue serotypes –> increases risk
dengue antibodies
IgG usually remains positive for life
antibodies do not give protection against dengue as more than one serotype but is not at increased risk of complication
pre renal causes of AKI
Drugs
Hypercalcaemia
Hypovolaemia (absolute and effect)
Drugs causing AKI
ACE/ARB
NSAIDS
cyclosporin
Tacrolimus
diagnosing Zollinger -Ellison syndrome
fasting serum gastrin level
Anti-Saccharomyces cerevisiae antibodies
A group of antibodies directed at components of the cell wall of the yeast Saccharomyces cerevisiae. Associated with chronic inflammatory bowel disease (particularly Crohn disease).
Schilling test
A test to determine the cause of B12 deficiency. Patients ingest radiolabelled B12 and then its urinary excretion is measured. Excretion will be normal if the cause is a dietary deficiency. If excretion is low (suggesting malabsorption), the test is repeated with orally administered intrinsic factor (IF). If excretion normalizes, the cause is IF deficiency. If excretion still remains low, the test is repeated with antibiotics, and then pancreatic enzymes to rule out bacterial overgrowth and pancreatic insufficiency, respectively.
p-ANCA
An autoantibody against myeloperoxidase granules (present in the perinuclear region of cytoplasm). p-ANCA levels are increased in patients with ulcerative colitis, autoimmune systemic vasculitis (especially Churg-Strauss syndrome and microscopic polyangiitis) and primary sclerosing cholangitis.
fecal lactoferrin
A marker of intestinal inflammation used to assess for, e.g., inflammatory bowel disease (IBD)
Whipple disease
An infectious disease caused by the bacteria Tropheryma whipplei. It is notoriously difficult to diagnose because of its variable presentation. Findings often include chronic malabsorptive diarrhea, weight loss, migratory non-deforming arthritis, lymphadenopathy, and a low-grade fever.
Tropical Sprue
A bacterial infection that is associated with a stay in the tropics or subtropics and leads to structural damage of the intestinal mucosa. Characterized by chronic diarrhea with subsequent malabsorption, abdominal cramps, progressive weight loss, and fatigue.
Hepatitis C
A viral infection that causes acute or chronic inflammation of the liver after an incubation period of 2 weeks to 6 months. Usually transmitted parenterally but can be transmitted sexually or perinatally. Inflammation is usually mild or not present at all and resolves within a few weeks or months. Can rarely cause acute liver failure. Often leads to chronic hepatitis.
test to confirm acute hepatitis A
Anti-HAV IgM
primary sclerosing cholangitis
Primary sclerosing cholangitis (PSC) is a progressive chronic inflammation of both the intrahepatic and extrahepatic bile ducts. While the exact etiology is unknown, there is a strong association with autoimmune diseases, particularly ulcerative colitis (UC). In the early stages, PSC is usually asymptomatic. Later in the course of the disease, patients present with symptoms of cholestasis (e.g., pruritus, jaundice). Laboratory abnormalities include elevated liver function tests and autoantibodies (pANCA in up to 80% of cases). Magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP) is performed to confirm the diagnosis. Management is primarily symptomatic, with liver transplantation reserved for end-stage liver disease.
hydatid cyst disease
A helminthic infection caused by cestodes of the genus Echinococcus (e.g., E. granulosus, E. multilocularis). Infection is typically acquired by accidental ingestion of Echinococcus eggs, which are shed in the feces of infected dogs. Infection results in cystic lesions in the liver (75% of cases), lung (15% of cases), and, rarely, other organs.
albendazole
An orally administered, broad-spectrum antihelminthic drug that is used to treat echinococcosis, cysticercosis, pinworm infection (enterobiasis), hookworm infection (ancylostomiasis, necatoriasis), ascariasis, trichuriasis, and strongyloidiasis. Mechanism of action: inhibition of microtubule synthesis.
HBsAg
Surface antigen
Protein on the surface of HBV; first evidence of infection
Anti‑HBs
Indicates immunity to HBV due to vaccination or resolved infection
Usually appears 1–3 months after infection.
HBcAg
Core antigen
Protein of the nucleocapsid
Anti‑HBc
Anti-HBC IgM indicates recent infection with HBV (≤ 6 months)
Anti-HBc IgG indicates resolved or chronic infections
HBeAg
Envelope antigen
Protein secreted by the virus that indicates viral replication and infectivity
Anti‑HBe
Indicates long-term clearance of HBV
Hepatitis A virus (HAV)
Picornavirus Non-enveloped virus Positive sense, single-stranded, linear RNA Fecal-oral 15–50 Acute hepatitis: fever, malaise, loss of appetite, nausea, abdominal pain, jaundice, ↑ AST/ALT Children < 6 years often have no symptoms Anti-HAV IgM Supportive Food and water hygiene Immunization Full recovery within ∼ 3 months Does not become chronic
IE - staphylococcus aureus
Most common cause of acute IE for all groups (including IV drug users and patients with prosthetic valves or pacemakers/ICDs)
Affects previously healthy valves
Usually fatal within 6 weeks (if left untreated)
IE - Viridans streptococci
Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve) and in prosthetic valves (≥ 60 days after surgery)
Common cause of IE following dental procedures
Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves
IE - Viridans streptococci
Most common cause of subacute IE, especially in predamaged native valves (mainly the mitral valve) and in prosthetic valves (≥ 60 days after surgery)
Common cause of IE following dental procedures
Produce dextrans that facilitate binding fibrin-platelet aggregates on damaged heart valves
Risk factors for chronic venous disease
Higher age and female sex (see “Epidemiology” above)
Family history of venous disease
Ligamentous laxity
Sedentary lifestyle and prolonged standing
Obesity
Pregnancy
Smoking
Prior thrombosis (postthrombotic syndrome)
Prior extremity trauma
Congenital abnormalities
primary prevention rheumatic fever
prompt antibiotic treatment (e.g., penicillin V) of GAS tonsillopharyngitis diagnosed by throat culture or rapid strep test
secondary prevention rheumatic fever
Antibiotic prophylaxis to prevent recurrence
Drug of choice: IM penicillin G benzathine
In patients with a penicillin allergy: oral macrolides
Usually administered every 28 days
Immediately follows antibiotic treatment of acute rheumatic fever (see “Treatment” above)
Duration depends on risk and severity of original episode
Rheumatic fever without carditis: 5 years or until the patient is age 21 (whichever is longer)
Rheumatic fever with carditis: 10 years or until the patient is age 21 (whichever is longer)
Rheumatic fever with carditis and permanent valvular heart defects: 10 years or until age 40 (whichever is longer)
