MEDD421 Final Exam Flashcards

1
Q

Why do closed chain kinetic exercised after ACL surgery?

A

because they reduce anterior-directed forced on the tibia relative to the femur and increase tibiofemoral compressive forces

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2
Q

Perimysium

A

The connective tissue that surrounds a bundle of muscle fibres.

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3
Q

A pathological fracture is one that…

A

Occurs in a bone that is already weakened due to underlying pathology

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4
Q

how much dietary Ca is needed daily?

A

1200 mg

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5
Q

What is the name of the main fibrinolytic enzyme generated by the use of tPA

A

plasmin

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6
Q

Explain the process of initial assessment of complaints suggestive of PE

A
  1. Assess using Wells and/or Geneva criteria
  2. Low or moderate probability (4 or lower) –> do a D-Dimer
  3. Positive D-Dimer or high probability proceed to CT
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7
Q

When to consult nephrology for dialysis

A
A- acidotic
E - electrolyte imbalance (hyperkalemia)
I - ingestion of toxic drugs 
O - volume overload
U - uremia (confusion, pericarditis)
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8
Q

What feature of creatinine makes it an imperfect marker for estimating glomerular filtration rate?

A

It is secreted by the renal tubules

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9
Q

Best imaging modality for renal colic

A

CT KUB

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10
Q

The issue with digoxin?

A

Narrow therapeutic range

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11
Q

what happens to bicarb in kidney disease?

A

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.

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12
Q

Grades of ligament injury

A

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

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13
Q

Stages of tendon and ligament healing

A

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)

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14
Q

Best imaging modality for superficial or dynamic muscle structures

A

US

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15
Q

Ottawa Knee Rule

A

Indicators for XR knee;

  • Age 55+
  • Isolated tenderness patella
  • cannot flex 90 degrees
  • unable to bear wt immediately and in ER for >4 steps
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16
Q

Pittsburgh knee rule

A

indicators for XR knee

  • <12 yrs or > 50 yrs
  • unable to walk 4 wt bearing steps
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17
Q

When would CT or MRI be indicated for knee injury?

A
  • 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)

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18
Q

Stages of knee rehab

A

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

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19
Q

Timeline for return to play after acl surgery

A

avg 6-12 mo after surgery. ~65% get back to same level of play

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20
Q

Crtieria for return to play post ACL surgery

A
  • no pain or swelling
  • full ROM
  • > 85% strength quads and hamstrings
  • psychological readiness
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21
Q

Estrogen and bone production/resorption?

A

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

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22
Q

denosumab

A

a mAb for RANK ligand - the ligand for the RANK receptors on osteoclasts. It mimics the action of osteoprotegrin

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23
Q

What is calcitriol and what does it do

A

active form of vitamin D. It works with PTH to increase levels of Ca in the blood.

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24
Q

3 major actions of PTH

A
  • 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.
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25
Q

Magnesium and Ca hemostasis

A

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.

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26
Q

2 major etiologies of hypercalcemia

A
  • Hyperparathyroidism (high PTH)

- Malignancy (low PTH)

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27
Q

Symptoms of hypercalcemia

A

Stones, bones, thrones, groans, and psychic overtones

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28
Q

Workup for hypocalcemia

A

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
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29
Q

Hypocalcemia with high PTH and high phosphate is likely related to

A

CKD

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30
Q

osteomalacia

A

Vitamin D deficiency

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31
Q

How much VIt D should adults >50 y with osteoporosis get?

A

800-1000 IU (compared to 400 IU recommended for other adults)

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32
Q

Osteoporosis definition

A

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

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33
Q

Imaging for osteoporosis

A

Dual Energy Absorptiometry (DXA) followed by comparisons of bone density to WHO population means. =/< -2.5 SD below mean is considered osteoporosis.

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34
Q

Treatment for osteoporosis

A

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
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35
Q

Primary hemostasis: Fxn and main players

A

Stop the bleeding!

VWF binds subendothelial collagen, platelets (platelet plug)

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36
Q

Secondary hemostasis: Main point of it, components and phases

A

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

37
Q

Fibrinoysis - main players and process

A

Plasminogen converted to plasmin by tPA

38
Q

Natural inhibitors of coagulation

A

Protein C and its cofactor Protein S.
Antithrombin
Tissue factor Pathway Inhibitor

39
Q

How does warfarin work?

A

Vitamin K antagonist. Many factors of coagulation are Vit K dependent - 10, 9, 7 and 2. These are all players of secondary hemostasis.

40
Q

Virchow’s triad

A

endothelial injury, stasis, hypercoagulability

==> VTE is likely

41
Q

Massive PE can cause ‘hemodynamic instability’ - what does that mean?

A

Circulatory shock and advanced heart failure.

Signs may include high troponin, arrhythmias, decreased BP, syncope, obvious shock

42
Q

Postthrombotic syndrome

A

a complication of DVT

Chronic venous insufficiency causes venous HTN, which can then cause edema, hypoxia, and inflammation.

43
Q

V/Q changes in PE

A

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

44
Q

DVT management

A

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

45
Q

Why do we need to overlap LMWH and warfarin?

A

LMWH acts more quickly and warfarin acts slowly. Warfarin also has a transient procoagulation effect by depleting protein C and S

46
Q

When to use tPA or surgery for VTE

A

Massive PE (patient is hemodynamically unstable)

47
Q

PESI criteria

A

estimates risk of complications following VTE

48
Q

Treatment for cancer-associated thrombosis

A

DOAC (not warfarin) or LMWH alone

49
Q

CHADS65

A

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.

50
Q

When would we use unfractionated heparin?

A

kidney failure because it isn’t renally excreted

51
Q

Cornerstone of CAD management

A

ASA (antiplatelet therapy)
Additional antiplatelet therapy (i.e., P2Y12 inhibitor) may be necessary for certain conditions such as acute coronary syndrome or stenting.

52
Q

The bladder, kidneys and genitalia develop from which germ layer(s)?

A

Kidney and genitalia develop from intermediate mesoderm.

Bladder develops from endoderm.

53
Q

Fats on urinalysis suggests

A

Nephrotic syndrome (fat increases due to loss and compensatory production of albumin)

54
Q

broad casts on urinalysis suggests

A

end stage chronic renal disease

55
Q

transitional epithelial cells on urinalysis suggests

A

lower UTI - transitional epithelial cells are in the lower urinary tract)

56
Q

bloody urine with RBC casts suggests

A

glomerulonephritis (ex: acute tubular necrosis)

57
Q

frothy urine suggests

A

protein in it - suggests nephrotic syndrome (things getting through filtration barrier)

58
Q

k+ management in the kidney

A

Majority of K+ is filtered but then it is mostly reabsorbed. Excretion of it depends on principals cells secreting K in the collecting duct.

59
Q

Things that modulate secretion of K at the principal cells (4)

A

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+

60
Q

3 main causes of hyperkalemia

A

1) increased intake
2) shift out of cells (occurs in insulin deficiency, metabolic acidosis, and digoxin toxicity)
3) impaired renal excretion (renal failure, hypoaldosteronism)

61
Q

Best imaging modality for hematuria

A

CT IVP (contrast; most sensitive)

62
Q

Explain the pre-renal, intrinsic and post-renal causes of AKI

A

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)

63
Q

Metabolic changes in AKI

A
  • 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.
64
Q

Severe complications of AKI (4)

A
  • pulmonary edema –> resp failure
  • Acidemia
  • hyperkalemia –> arrhythmias
  • uremic complications (pericarditis, encephalopathy, seizures)
65
Q

2 main patterns of glomerular nephritis

A

1) NephrOtic syndrome - filtration barrier compromised

2) NephrItic syndrome - diffuse inflam of glomerulus

66
Q

Screening for CKD

A

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
67
Q

utility of imaging in CKD workup

A

To rule out postrenal causes (sclerosis/fibrosis of kidney, pyelonephritis, blockage, BPH)

68
Q

Complications of CKD and when do they begin? (acronym)

A
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)
69
Q

Management of CKD

A

Control BP and reduce proteinuria:

  • 1st line: ARB or ACEi
  • Diet changes (Na < 2g per day)

Manage comorbidities and risk factors

70
Q

midline cerebellar disease (lesion to vermis) presents with

A
  • Gait issues and truncal imbalance
  • head tilt
  • nystagmus
71
Q

Lesion to flocculonodular lobe of cerebellum presents with

A
  • truncal ataxia (reeling of trunk from side to side; wide stance)
  • nustagmus
72
Q

Lateral cerebellar disease (both hemispheres and posterior lobe of cerebellum) presents with

A
  • dysmetria (overshooting)

- dysdiadodyskinesia (poor rapid alternating movements)

73
Q

Lesion to anterior cerebellar lobe presents with

A

gait ataxia

Can occur with acute (passive) chronic EtOH intake (enduring).

74
Q

Neuroleptic malignant syndrom

A

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

75
Q

clinical diagnosis of parkinson’s

A

Bradykinesia (slow initiation, progressive decreased amplitude)
+
(possible) Rigidity, rest tremor, instability

76
Q

Mainstay of Parkinson’s therapy

A

Levodopa with carbidopa

77
Q

Amantadine

A

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

78
Q

The problem with dopamine agonists

A

~10% develop impulse control disorders

79
Q

WHich neural circuit is implicated in schizophrenia

A

limbic circuit

Specifically the mesolimbic pathway

80
Q

differentiate D1 and D2 receptors

A

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.

81
Q

Almost all antipsychotic meds block what

A

D2 receptors.

82
Q

What are the four dopaminergic pathways in the brain and how are they implicated in schizophrenia

A

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)

83
Q

Differentiate 1st, 2nd, and 3rd generation antipsychotic mechanisms of action

A

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

84
Q

Clozapine

A

A 2nd generation antipsychotics that should be reserved for treatment-refractory psychosis

85
Q

Which of the three generations of antipsychotics is ‘best’?

A
  • Perform the same for treating +ve sx
  • 3rd generation better for treating -ve sx due to partial DA agonism
  • All have unique SEs
86
Q

(general) Adverse effects of 1st and 2nd generation antipsychotics

A

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)
87
Q

Treating acute dystonic reaction to antipsychotics

A

ABCs

Benztropine or diphenhydramine

88
Q

Akathisia

A

Movement disorder characterized my inner restless and strong need to be in constant emotion. Can be a SE of antipsychotic treatment.

89
Q

4 major SEs of antipsychotics

A

1) acute dystonia
2) pseudo-parkinsonism
3) akathisia
4) tardive dyskinesia