MEDD421 Final Exam Flashcards
Why do closed chain kinetic exercised after ACL surgery?
because they reduce anterior-directed forced on the tibia relative to the femur and increase tibiofemoral compressive forces
Perimysium
The connective tissue that surrounds a bundle of muscle fibres.
A pathological fracture is one that…
Occurs in a bone that is already weakened due to underlying pathology
how much dietary Ca is needed daily?
1200 mg
What is the name of the main fibrinolytic enzyme generated by the use of tPA
plasmin
Explain the process of initial assessment of complaints suggestive of PE
- Assess using Wells and/or Geneva criteria
- Low or moderate probability (4 or lower) –> do a D-Dimer
- Positive D-Dimer or high probability proceed to CT
When to consult nephrology for dialysis
A- acidotic E - electrolyte imbalance (hyperkalemia) I - ingestion of toxic drugs O - volume overload U - uremia (confusion, pericarditis)
What feature of creatinine makes it an imperfect marker for estimating glomerular filtration rate?
It is secreted by the renal tubules
Best imaging modality for renal colic
CT KUB
The issue with digoxin?
Narrow therapeutic range
what happens to bicarb in kidney disease?
Bicarb goes down because it is being used up to buffer the high levels of acid that are retained in the body as they can’t be filtered out anymore.
Grades of ligament injury
I - sprain - stretched but fibres intact
II - partial rupture but there is an endpoint to stretch on physical exam
III - complete rupture, lost fxn, no endpoint
Stages of tendon and ligament healing
1) Inflammatory (~1wk; recruitment of inflam mediators)
2) Proliferative (several weeks; Fibroblasts proliferate and type III collagen is laid down [scar tissue]; more vascular)
3) remodelling (weeks-months; Fibres become more organized; shift from type III to type I collagen; less vascularized; less cellular)
Best imaging modality for superficial or dynamic muscle structures
US
Ottawa Knee Rule
Indicators for XR knee;
- Age 55+
- Isolated tenderness patella
- cannot flex 90 degrees
- unable to bear wt immediately and in ER for >4 steps
Pittsburgh knee rule
indicators for XR knee
- <12 yrs or > 50 yrs
- unable to walk 4 wt bearing steps
When would CT or MRI be indicated for knee injury?
- Tibial plateau fracture
- No fracture found on XR and you suspect an occult fracture or internal derangement
- Suspicion of additional injury
MRI indicated if suspicion of deep ligament injury (i.e., ACL)
Stages of knee rehab
0: Prehabilitation - before surgery decrease swelling and pain, achieve normal gait and RoM
1: Immediate post-op manage pain and get RoM, strength and walking as tolerated
2: Functional strengthening and prepare for return to play.
3: Return to play
Timeline for return to play after acl surgery
avg 6-12 mo after surgery. ~65% get back to same level of play
Crtieria for return to play post ACL surgery
- no pain or swelling
- full ROM
- > 85% strength quads and hamstrings
- psychological readiness
Estrogen and bone production/resorption?
Estrogen stimulates osteoblasts, which stimulate osteoprotegrin, which is a sequestering protein. It sequesters the RANK ligand to prevent it from binding RANK receptors on osteoclasts
denosumab
a mAb for RANK ligand - the ligand for the RANK receptors on osteoclasts. It mimics the action of osteoprotegrin
What is calcitriol and what does it do
active form of vitamin D. It works with PTH to increase levels of Ca in the blood.
3 major actions of PTH
- Promotes Ca reabsorption at distal renal tubule
- Promotes renal activation of vitamin D (increases Ca levels in blood)
- Regular episodic release of PTH promotes bone growth and mineral deposition. At sustained levels, PTH promotes bone resorption.
Magnesium and Ca hemostasis
Hypomagnesemia can reduce PTH secretion or cause PTH resistance. PTH is responsible for increasing Ca reabsorption. Remember to check and correct Mg igf hypocalcemia is present.
2 major etiologies of hypercalcemia
- Hyperparathyroidism (high PTH)
- Malignancy (low PTH)
Symptoms of hypercalcemia
Stones, bones, thrones, groans, and psychic overtones
Workup for hypocalcemia
Check Ca, PTH and Mg.
- Low Mg can cause hypocalcemia
- PTH will be low if hypocalcemia is due to surgery, autoimmune, congenital hypoplasia/mutation
- PTH will be high if hypocalcemia is due to Vit D deficiency, CKD, sepsis, hemorrhage/surgery
Hypocalcemia with high PTH and high phosphate is likely related to
CKD
osteomalacia
Vitamin D deficiency
How much VIt D should adults >50 y with osteoporosis get?
800-1000 IU (compared to 400 IU recommended for other adults)
Osteoporosis definition
Low bone mass AND microarchitectural deterioration with a consequent increase in bone fragility and susceptibility to fracture.
T score =/< -2.5 SD below mean BMD
Imaging for osteoporosis
Dual Energy Absorptiometry (DXA) followed by comparisons of bone density to WHO population means. =/< -2.5 SD below mean is considered osteoporosis.
Treatment for osteoporosis
Use FRAX score to decide who is at risk of fracture and requires treatment.
- Lifestyle, Ca and Vit D supplementation
- Bisphosphonates (anti-resorpative) first line
- Denosumab (RANK L mAb) 2nd line
Primary hemostasis: Fxn and main players
Stop the bleeding!
VWF binds subendothelial collagen, platelets (platelet plug)
Secondary hemostasis: Main point of it, components and phases
Propagation of the coagulation cascade to make a better clot.
Phase 1: Initiation = Intrinsic pathway. Tissue factor -…-> some thrombin
Phase 2: Amplification/propagation = extrinsic pathway. Massive thrombin production
Phase 3: Fibrin clot/stabilization. Thrombin converts fibrinogen to fibrin
Fibrinoysis - main players and process
Plasminogen converted to plasmin by tPA
Natural inhibitors of coagulation
Protein C and its cofactor Protein S.
Antithrombin
Tissue factor Pathway Inhibitor
How does warfarin work?
Vitamin K antagonist. Many factors of coagulation are Vit K dependent - 10, 9, 7 and 2. These are all players of secondary hemostasis.
Virchow’s triad
endothelial injury, stasis, hypercoagulability
==> VTE is likely
Massive PE can cause ‘hemodynamic instability’ - what does that mean?
Circulatory shock and advanced heart failure.
Signs may include high troponin, arrhythmias, decreased BP, syncope, obvious shock
Postthrombotic syndrome
a complication of DVT
Chronic venous insufficiency causes venous HTN, which can then cause edema, hypoxia, and inflammation.
V/Q changes in PE
Both high V/Q (places where venitaltion is happening but clot stops perfusion) and low V/Q (places where atelectasis has occurred and returned blood flow). Low V/Q predominates
DVT management
1st line) LMWH + Warfarin for 5 days.
2nd line) DOAC (Dabigatran is antithrombin and others are anti Factor Xa)
Continue treatment for at least 3 mo and then follow Men Continue and HERDOO2 criteria
Why do we need to overlap LMWH and warfarin?
LMWH acts more quickly and warfarin acts slowly. Warfarin also has a transient procoagulation effect by depleting protein C and S
When to use tPA or surgery for VTE
Massive PE (patient is hemodynamically unstable)
PESI criteria
estimates risk of complications following VTE
Treatment for cancer-associated thrombosis
DOAC (not warfarin) or LMWH alone
CHADS65
Indications for oral anticoagulation in atrial fibrillation patients
- CHF
- HTN
- Age >65
- Diabetes
- Stroke or TIA
All of these get OAC. If just CAD or other vascular disease then ASA is okay.
When would we use unfractionated heparin?
kidney failure because it isn’t renally excreted
Cornerstone of CAD management
ASA (antiplatelet therapy)
Additional antiplatelet therapy (i.e., P2Y12 inhibitor) may be necessary for certain conditions such as acute coronary syndrome or stenting.
The bladder, kidneys and genitalia develop from which germ layer(s)?
Kidney and genitalia develop from intermediate mesoderm.
Bladder develops from endoderm.
Fats on urinalysis suggests
Nephrotic syndrome (fat increases due to loss and compensatory production of albumin)
broad casts on urinalysis suggests
end stage chronic renal disease
transitional epithelial cells on urinalysis suggests
lower UTI - transitional epithelial cells are in the lower urinary tract)
bloody urine with RBC casts suggests
glomerulonephritis (ex: acute tubular necrosis)
frothy urine suggests
protein in it - suggests nephrotic syndrome (things getting through filtration barrier)
k+ management in the kidney
Majority of K+ is filtered but then it is mostly reabsorbed. Excretion of it depends on principals cells secreting K in the collecting duct.
Things that modulate secretion of K at the principal cells (4)
1) aldosterone - increases Na reabsorption and K secretion
2) Tubular flow rate - higher secretion
3) Amount of Na in collecting duct - higher effective Na increases Na reabsorption which then increases K secretion
4) Acid-base - High H+ - H+ secreted instead of K+
3 main causes of hyperkalemia
1) increased intake
2) shift out of cells (occurs in insulin deficiency, metabolic acidosis, and digoxin toxicity)
3) impaired renal excretion (renal failure, hypoaldosteronism)
Best imaging modality for hematuria
CT IVP (contrast; most sensitive)
Explain the pre-renal, intrinsic and post-renal causes of AKI
Pre-renal: Issue with perfusion to the kidney causing low GFR. May be decreased absolute ECF (fluid loss) or effective ECF (poor perfusion)
Intrinsic: Damage to kidneys (inflammatory)
Post-Renal: Blockage (kidney stones)
Metabolic changes in AKI
- Metabolic ACIDOSIS: Ineffective excretion of H+ and decrease HCO3 as it is used up to buffer the acid.
- Increased Ca, K, and decreased PO4 to compensate for acid.
Severe complications of AKI (4)
- pulmonary edema –> resp failure
- Acidemia
- hyperkalemia –> arrhythmias
- uremic complications (pericarditis, encephalopathy, seizures)
2 main patterns of glomerular nephritis
1) NephrOtic syndrome - filtration barrier compromised
2) NephrItic syndrome - diffuse inflam of glomerulus
Screening for CKD
Screen every year starting at age 60 or if risk factors present:
- HTN, diabetes, atherosclerosis
- FHx
- High risk ethnicity (FN, South Asian, Pacific Islander)
- Unexplained anemia (normocytic)
- CHF
- Longterm or high dose NSAID use
- Recurrent UTIs or pyelonephritis
utility of imaging in CKD workup
To rule out postrenal causes (sclerosis/fibrosis of kidney, pyelonephritis, blockage, BPH)
Complications of CKD and when do they begin? (acronym)
Begin around stage 3 (GFR<60) MADHUNGER - Metabolic Acidosis - Dyslipidemia - Hyperkalemia - Uremia (solute and fluid retention sx) - Na/H2O retention (edema, HTN) - Growth retardation and developmental concenrs - EPO failure - Renal osteodystrophy (Ca, Vit D, PTH dystregulation)
Management of CKD
Control BP and reduce proteinuria:
- 1st line: ARB or ACEi
- Diet changes (Na < 2g per day)
Manage comorbidities and risk factors
midline cerebellar disease (lesion to vermis) presents with
- Gait issues and truncal imbalance
- head tilt
- nystagmus
Lesion to flocculonodular lobe of cerebellum presents with
- truncal ataxia (reeling of trunk from side to side; wide stance)
- nustagmus
Lateral cerebellar disease (both hemispheres and posterior lobe of cerebellum) presents with
- dysmetria (overshooting)
- dysdiadodyskinesia (poor rapid alternating movements)
Lesion to anterior cerebellar lobe presents with
gait ataxia
Can occur with acute (passive) chronic EtOH intake (enduring).
Neuroleptic malignant syndrom
A drug-induced dystonia that can occur with neuroleptic exposure. Can also occur with abrupt withdrawal of levodopa or DA agonists.
Characterized by tetrad of encephalopathy, rigidity, hyperthermia, and dysautonomia
clinical diagnosis of parkinson’s
Bradykinesia (slow initiation, progressive decreased amplitude)
+
(possible) Rigidity, rest tremor, instability
Mainstay of Parkinson’s therapy
Levodopa with carbidopa
Amantadine
usually used as a flu treatment but is can provide sild benefit for tremor and dyskinesias. Can be used in early parkinson’s or an adjunct later in parkinsons
The problem with dopamine agonists
~10% develop impulse control disorders
WHich neural circuit is implicated in schizophrenia
limbic circuit
Specifically the mesolimbic pathway
differentiate D1 and D2 receptors
D1 receptors are excitatory - reinforce target-oriented and rewarding behaviour
D2 receptors are inhibitory - they counteract the indirect motor (inhibiting) pathway and allow some superfluous movements to come through.
Almost all antipsychotic meds block what
D2 receptors.
What are the four dopaminergic pathways in the brain and how are they implicated in schizophrenia
1) Mesolimbic (reward and emotions –> +ve sx in psychosis)
2) Mesocortical (cognition and exec function –> -ve sx in schizophrenia)
3) Nigrostriatal pathway (projects to basal ganglia to control motor outputs –> tremors when treated with antipsychotics)
4) tuberoinfundibular pathway (controls prolactin secretion when DA is inhibited)
Differentiate 1st, 2nd, and 3rd generation antipsychotic mechanisms of action
1st: Block D2 receptors. SEs arise due to action on H1, alpha1 and M1 receptors
2nd: Same action as 1st generation with additional action on 5HT receptors.
3rd: Same action as 2nd generation with additional partial agonism of DA which reduces some adverse effects and symptoms
Clozapine
A 2nd generation antipsychotics that should be reserved for treatment-refractory psychosis
Which of the three generations of antipsychotics is ‘best’?
- Perform the same for treating +ve sx
- 3rd generation better for treating -ve sx due to partial DA agonism
- All have unique SEs
(general) Adverse effects of 1st and 2nd generation antipsychotics
These are D2 antagonists
- D2 action on mesocortical pathway –> exacerbates -ve sx
- D2 action in nigrostriatal pathway –> extrapyramidal sx
- D2 action in tuberoinfundibular pathway –> release inhibition of prolactin release
- H1 action –> sedation, wt gain
- alpha1 action –> low BP, dizziness, drowsiness
- M1 –> anticholinergic sx (dry mouth, urinary retention, blurred vision, constipation)
Treating acute dystonic reaction to antipsychotics
ABCs
Benztropine or diphenhydramine
Akathisia
Movement disorder characterized my inner restless and strong need to be in constant emotion. Can be a SE of antipsychotic treatment.
4 major SEs of antipsychotics
1) acute dystonia
2) pseudo-parkinsonism
3) akathisia
4) tardive dyskinesia
