Clinical Physiology Flashcards
Types of JVP waveforms
A wave: atrial contraction
C wave: Pushing of tricuspid valve towards right atrium, carotid pulsation of neck
V wave: Venous return, filling of right atrium
X wave: Relaxation of right atrium
Y wave: Emptying of right atrium
Pathologic JVP waveforms:
Absent A wave
Atrial fibrillation
Pathologic JVP waveforms:
Large A wave
Reduced RV compliance —> require more contraction from RA
Pulmonic stenosis
Pulmonary HTN
Pathologic JVP waveforms:
Large v wave
Backflow of blood to RA —> more blood pumped from RA to RV
Tricuspid regurgitation
Pathologic JVP waveforms:
Absent Y wave
Cardiac tamponade (obstructive shock)
Pathologic JVP waveforms:
Cannon a wave
RA contraction against a closed tricuspid valve
Complete heart block (3rd degree AV block pumped from RA to fill RV)
Aortic stenosis carotid pulse configuration
Pulsus parvus et tardus
(Pulse that is small and slow)
AORTIC STENOSIS
Pulsus Bisferiens (2 peaks in systole or triple cadence beat if with S4) is seen in?
HOCM
severe aortic regurg
Early part of diastole:
S3 or S4?
S3 (increasing filling pressure, systolic HF)
S4 is in late diastole (ventricular noncompliance, diastolic HF)
Most common type of ASD
Secundum
Wide splitting of S2
Delay in closure of PV - right side of heart)
• RBBB
• Pulmonic stenosis
Paradoxical or reversed splitting of S2
Delay closure in AV - left side of heart
LBBB
Aortic stenosis
HOCM
MI
mL for acute tamponade
200 ml
mL for chronic tamponade
2000 mL
Cardiac tamponade Triad
Beck’s Triad
• Muffled heart sounds
• Distended neck veins
• Hypotension
*Absent Y wave
*Prominent X wave
Acute MI of inferior wall of LV activated reflex
Bezold-Jarisch reflex
1. Bradycardia
2. Hypotension
3. Hypopnea/apnea
Due to activation of parasympathetic pathways in inferior wall of LV
Acute MI of anterior wall of LV activated reflex
James reflex
1. Tachycardia
2. Hypertension
3. Hyperapnea
Due to activation of sympathetic pathways in anterior wall of LV
Cerebral perfusion pressure (CPP) formula
CPP = MAP - ICP
Cushing reflex
- Hypertension
- Bradycardia
- Hypopnea/Apnea
- due to increased MAP (to make it greater than ICP) and subsequent activation of baroreceptor reflex leading to bradycardia and hypopnea/apnea
Levels of Hyperkalemia in ECG:
Tall-peaked T-waves
5.5 - 6.5 mM
Levels of Hyperkalemia in ECG:
Loss of P waves
6.5 - 7.5 mM
Levels of Hyperkalemia in ECG:
Widened QRS complex
7.0-8.0 mM
hypokalemia in ECG:
Prominent U waves
Hypocalcemia in ECG
Prolonged QT interval
Hypercalcemia in ECG
Shortened QT interval
AV blocks
Bradycardia
Abnormal fast accessory conduction pathway from atria to ventricles (bypass AV node)
Bundle of Kent
Most common type of ventricular preexcitatiin syndrome
Wolff-Parkinson White Syndrome
3 components
1. Delta wave
2. Shortened PR interval
3. Widened QRS complex
Renal tubular defect in PCT
Fanconi syndrome
*Generalized absorption defect in PCT —> excretion of AAs, glucose, HCO3 And PO4, and all other substances
Renal tubular defect in TAL of LH
Bartter syndrome
*Na-K-Cl cotransporter defect
Renal tubular defect in DCT
Gitelman syndrome
*NaCl reabsorption defect
Renal tubular defect in Late CD
Liddle syndrome
*Gain of function mutation —> dec. Na channel degradation —> inc Na reabsorption —> HTN
Syndrome of apparent mineralocorticoid excess (SAME)
*deficienct if 11-beta hydroxysteroid dehydrogenatse type 2 (11-B-HSD) —> inc cortisol —> inc mineralocorticoid activity —> aldosterone inc Na and dec K
What is order of renal tubular defect
Fanconi’s BaGeLS
Role of 11-Beta hydroxysteroid dehydrogenase Type 2
Convert cortisol to cortisone (inactive form)
Effects of Fanconi syndrome
Metabolic acidosis
Hyposphatemia
Osteopenia
Bartter syndrome versus Gitelman syndrome
Similarities:
Autosomal recessive
Metabolic alkalosis and Hypokalemia
Differences
*Mg and Ca
Bartter: Normal Mg, Hypercalciuria
Gitelman: HypoMg, Hypocalciuria
Neprolith
Bartter: High risk
Gitelman: Low risk
Mimics
Bartter: Chronic loop diuretic use
Gitelman: Chronic thiazide diuretic use
Intake of _____________ can cause SAME because it contains ____________ that blocks ______________
Licorice; Glycyrrhetinic acid; 11-B-Hydroxysteroid Dehydrogenase Type 2 (11-B-HSD)
Liddle is _______________disorder while SAME is ___________disorder
Autosomal dominant; Autosomal recessive
Liddle and SAME cause the ff effects
Metabolic Alkalosis
Hypokalemia
HTN
Hypoaldosteronism
Decorticate and Decrebrate motor GCS
M3; M2
Cerebellar lesions affect the ____________ side
Ipsilateral
Presentation of cerebellar lesions in:
Flocculonodular lobe
Cerebellar nystagmus
Presentation of cerebellar lesions in:
Deep cerebellar nuclei (Dentate, Emboliform, Globose, Fastigial nuclei)
Hypotonia
Presentation of cerebellar lesions in:
Cerebellar vermis
Truncal ataxia (middle, midline)
Presentation of cerebellar lesions in:
Cerebellar hemisphere
Ipsilateral intention tremor
Dysdiadochokinesia
Falls toward side of lesion
Lesions of Basal Ganglia:
Globus Pallidus
Athetosis
(Writhing movements of hand, arm, and neck)
Presentation of cerebellar lesions in:
Subthalamus
Hemiballismus
(Sudden flailing movements of an entire limb)
Presentation of cerebellar lesions in:
Putamen
Chorea
(Flicking movements of hands, face, body)
Presentation of cerebellar lesions in:
Substansia nigra
Parkinsons Dse
Resting tremor
Rigidity
Akinesia
Postural instability
Presentation of cerebellar lesions in:
Striatum (Caudate nucleus + Putamen)
Huntington dse
(Chorea, neurodegeneration)
Brain lesion in dominant parietal cortex will cause?
Gerstmann syndrome
1. Agraphia
2. Acalculia
3. Finger agnosia
4. Left-right disorientation
Brain lesion in nondominant parietal cortex will cause?
Hemispatial neglect syndrome
Agnosia of contralateral side
Syndrome caused by Mamillary bodies damage
Wernicke-Korsakoff syndrome (Vitamin B1 deficiency through chronic alcoholism)
Wernicke (reversible) CANO
Confusion
Ataxia
Nystagmus
Ophthalmoplegia
Korsakoff (irreversible)
Confabulation
Personality changes
Syndrome caused by damage to Amygdala
Kluver Blucy Syndrome
(HSV-1, temporal lobe encephalitis)
Disinhibited behavior
Hyperphagia
Hypersexual
Hyperoral
Caused by damage to Reticular activating system
Coma
Reduced arousal and wakefulness
Syndrome associated with dorsal midbrain pathology
Parinaud syndrome (pinealoma - close to superior colliculus)
1. Vertical gaze palsy
2. Lid retraction
3. Pupillary light near dissociation
4. Convergence retraction nystagmus
FEV/FVC ratio to dx Obstructive lung dse
<70%
Chronic bronchitis clinical dx is: daily productive cough of ____________ months or more, in at least _________ consecutive years
3; 2
Characteristic of dse in 17-alpha hydroxylase deficiency
HTN
Hypernatrenia
Hypokalemia
No virilization
Low cortisol, low sex hormones, inc mineralocorticoids
Bilateral adrenal hyperplasia due to negative feedback from low cortisol —> high ACTH
Hyperpigmentation due to negative feedback from low cortisol —> high POMC —> high ACTH —> high MSH
Characteristic of dse in 21-alpha hydroxylase deficiency
Normal BP
Normal NA
Normal K
Virilization in females, ambiguous genitalia in males
Low cortisol, elevated sex hormones, low mineralocorticoids
Bilateral adrenal hyperplasia due to negative feedback from low cortisol —> high ACTH
Hyperpigmentation due to negative feedback from low cortisol —> high POMC —> high ACTH —> high MSH
Characteristic of dse in 11-beta hydroxylase deficiency
HTN
Hypernatrenia
Hypokalemia
Virilization in females, ambiguous genitalia in males
Low cortisol, elevated sex hormones, low mineralocorticoids (but elevated 11-deoxycortisone)
Bilateral adrenal hyperplasia due to negative feedback from low cortisol —> high ACTH
Hyperpigmentation due to negative feedback from low cortisol —> high POMC —> high ACTH —> high MSH
Common presentations of hyper and hypo thyroid
AUB
Dec libido
Infertility
Proximal myopathy
Pretibial myxedema
