Cumulative Uworld Notes Flashcards

1
Q

How does CMV virus infect?

A
  • CMV can be acquired thru transfusion of leukocyte-laden blood products, as the virus infects leukocytes of granulocyte that are its defining characteristics
    • Encapsulated, lactose fermenting, gram-negative bacillus that appears mucoid in culture.
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2
Q

Draw out characteristics of gram-negative bacteria

A

?

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3
Q

Explain the symptoms of bipolar disorder.

A
  • Irritable mood, hyperactivity, pressured speech, DEC need for sleep, and grandiose delusions = manic episode. Patients with one or more lifetime manic episodes have bipolar I disorder. Manic episodes can occur WITH or WITHOUT psychotic features (i.e. delusions, hallucinations).
  • Delusions, if presents, are mood congruent (grandiose themes involving special talent and powers) but can also be mood incongruent. Most bipolar I patients will experience both major depressive and manic episodes, but depressive episodes are NOT required for diagnosis
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4
Q

What is positive predictive value? (PPV)

A

-Answers the question: If the test result is positive, what is the probability that a pt. has the disease? PPV is calculated as the proportion of subject who truly have the disease among all those with a positive test result.

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5
Q

What is negative predictive value (NPV)?

A

-Answers the question: If the test result is negative, what is the probability that a pt. doesn’t have the disease? It is calculated as a proportion of subjects who are truly free of disease among all those with a negative test result.

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6
Q

What is oppositional defiant disorder? How does it differ from antisocial, borderline, or conduct disorder?

A
  • Oppositional defiant disorder: behavioral disorder of childhood characterized by argumentative and defiant behavior toward authority figures. It does NOT involve the more severe violations of the basic rights of others seen in conduct disorder
  • Antisocial personality disorder: characterized by a pattern of disregard for and violation of the rights of others and is not diagnosed in individuals under age 18.
  • Borderline personality disorder involves a pervasive pattern of marked impulsivity, unstable moods and relationships, and recurrent suicidal behavior or self-mutilation.
  • conduct disorder involves behaviors that are more severe and aggressive than oppositional defiant disorder (ODD). Think physical aggression, or cruelty towards people or animals, destruction of property, or typical pattern of stealing or deceit.
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7
Q

Explain MOA of trazodone

A

-Serotonin modulator (antagonizes postsynaptic serotonin receptors and inhibits serotonin reuptake) and has minimal effects on NE and dopamine. Additional properties include α-adrenergic blockade (can cause orthostatic hypotension and priapism), and histamine H1 receptor antagonism that may underlie its sedating effect.

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8
Q

Explain what a crossover study is

A

-In crossover study, subjects are randomly allocated to a sequence of 2 or more treatments given consecutively. A washout (not treatment) period is often added between treatment intervals to limit the confounding effects of prior treatment.

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9
Q

What is a drawback of crossover trials? What is done to counteract this?

A
  • the effects of one treatment may “carry over” and alter the response to subsequent treatments.
  • The washout period is designed to be long enough to allow the effects of prior treatment to wear off
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10
Q

What is a case-control study?

A

-Designed by selecting patients with a particular disease (cases) and without the disease (controls) and then determining their previous exposure status

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11
Q

What is a case series?

A

A descriptive study that tracks patients with a known condition (i.e. particular exposure, risk factor, or disease) to document natural history or response to treatment. Unlike case-control, a case series is a qualifying study that cannot quantify statistical significance

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12
Q

What is a cross-sectional study?

A

AKA prevalence study. Characterized by the simultaneous measurement of exposure and outcome. It is a snapshot study design that frequently uses surveys. Are inexpensive and easy to perform

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13
Q

What is a prospective cohort study?

A

Are organized by selecting a group of individuals (i.e. cohort), determining their exposure status, and then following them over time for development of the disease of interest. Sometimes the exposure status is determined retrospectively and patients are tracked from the point of exposure onward, typically using medical records.

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14
Q

Explain what odds ratio is

A

It is a measure of association between an exposure and an outcome. Represents the odds that an outcome occurred in the presence of a particular exposure compared to the odds that the outcome occurred in the absence of that exposure. Used in case-control studies.

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15
Q

What is relative risk?

A

Risk of disease in the exposed divided by risk of disease in the non-exposed.

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16
Q

What are the stages of change?

A

1) Precontemplation: not thinking about behavior modification
2) Contemplation: Thinking about behavior modification
3) Preparation: Planning behavior modification
4) Action: Putting plan into action
5) Maintenance: maintaining new behavior

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17
Q

What is a confounder bias? How is it controlled so it doesn’t affect outcome?

A
  • A confounder is associated with both exposure and outcome and affects the measure of association between exposure and outcome, such that there initially appears to be a statistically significant association between the 2 on crude analysis (ex: shoe size INC, IQ INC). However, once the results are stratified by the confounding variable, the association disappears.
  • Matching is used in case-control studies in order to control confounding. Matching variables should always be the potential confounders of the study (i.e. age, race). Cases and controls are then selected based on matching variables so that both groups have a similar distribution in accordance with the variables.
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18
Q

What is conversion disorder?

A
  • Neurologic symptom incompatible with any known neurologic disease; often acute onset associated with stress. It is a type of somatic symptom disorder characterized by symptoms or deficits of voluntary motor and/or sensory function that are incompatible with any recognized neurological condition and can’t be explained by another medical or mental disorder.
  • Symptoms must be neurological and include weakness, paralysis, gait disturbance, blindness, diplopia, aphonia, anesthesia, and seizures (aka psychogenic or non-epileptic seizures).
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19
Q

Why can’t incidence measures be directly measured in case-control studies?

A

Incidence measures (i.e. relative risk or relative rate) can’t be directly measured in case-control studies b/c the people being studied are those who already have the disease. Relative risk and relative rate are calculated in COHORT studies, in which people are followed over time for developing the disease

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20
Q

What is risk and how is it calculated?

A
  • Risk is the probability of developing a disease over a certain period of time.
  • Calculate by dividing the number of affected subjects by the total number of subjects in the corresponding exposure group
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21
Q

What is the treatment of choice for OCD?

A

Serotonergic antidepressants (SSRIs)

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22
Q

What is acetylcholine involved in, in the CNS? Degeneration of it is associated with what pathology?

A

ACh is involved primarily in arousal, memory, and learning. Degeneration of cholinergic neurons is associated with Alzheimer dementia

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23
Q

What is norepinephrine involved in terms of psychiatrics? What pathophysiology is it associated with when NE levels are DEC? What other neurotransmitter is involved with this particular pathogenesis?

A

-NE is a catecholamine involved in mood, anxiety, alertness, learning, and memory. DEC neurotransmission of NE and serotonin has been implicated in pathophysiology of depression.

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24
Q

Which of the following factors most INC a patient’s risk of dying by suicide?

a) Access to firearms
b) Acute illness with pain
c) Age
d) Marijuana usage
e) Marital status

A

The majority of complete suicides occur with the use of a firearm. Access to guns significantly INC risk of death by suicide.

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25
Q

What medication is most appropriate agent for long term management of a patient with bipolar disorder?

A

Valproate (anticonvulsant) has mood stabilizing properties and is an effective maintenance treatment of bipolar disorder

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26
Q

How do you diagnose schizophrenia?

A

Requires greater than or equal to 2 of the following 5 symptoms: delusions, hallucinations, disorganized speech, grossly disorganized behavior, and negative symptoms. One of these must be delusions, hallucinations, or disorganized speech. Total illness duration must be greater than or equal to 6 months (including prodromal and residual periods) with greater than or equal to 1 month of active symptoms

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27
Q

Pyruvate dehydrogenase picmonic

A

http://www.picmonic.com/learn/pyruvate-dehydrogenase-deficiency_151

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28
Q

G6PD deficiency

A

http://www.picmonic.com/learn/g6pd-deficiency_436

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29
Q

G6PD mechanism

A

http://www.picmonic.com/learn/g6pd-mechanism_438

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30
Q

Neural plate gives rise to what?

A

Neural tube and neural crest cells

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31
Q

Notochord becomes what?

A

Nucleus pulposus of intervertebral disc in adults

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32
Q

Forebrain (prosencephalon) becomes what?

A

1) Telencephalon -> cerebral hemispheres (walls) and Lateral ventricles (cavities)
2) Diencephalon -> Thalamus, hypothalamus (walls) and Third ventricle (cavities)

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33
Q

Midbrain (mesencephalon) becomes what

A

Mesencephalon -> Midbrain (walls) and Aqueduct (cavities)

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34
Q

Hindbrain (rhombencephalon)

A

1) Metencephalon -> Pons and cerebellum (walls) and upper part of fourth ventricle
2) Myelencephalon -> Medulla (walls) and lower part of fourth ventricle (cavities)

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35
Q

Where are serotonin releasing neurons located in the CNS?

A

Raphe nuclei

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36
Q

Antidepressants such as selective serotonin reuptake inhibitors, serotonin norepinephrine reuptake inhibitors, and tricyclic antidepressants inhibit serotonin reuptake at which synapses?

A

Raphe nucleus (of the brainstem)

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37
Q

Where is the raphe nuclei located in and what role does it have?

A

Raphe nuclei is located in pons, midbrain, and medulla, and axons from these cell bodies project throughout CNS to synapse on cerebral cortex, thalamus, hypothalamus, cerebellum, hippocampus, and spinal cord.

These neurons play role in sleep-wake cycle, anxiety, mood, psychosis, sexuality, eating behavior, and impulsivity.

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38
Q

The caudate nucleus and putamen form what structure and what role does that structure have? Give an example of a pathology associated with it.

A

Caudate nucleus and putamen form the STRIATUM which functions in motor activities.

Huntington disease, there is loss of cholinergic and GABA-releasing neurons in striatum

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39
Q

What does the locus ceruleus house? (think neurotransmitter). Where is it located?

A

Houses norepinephrine-secreting neurons that participate in activation of “fight or flight” response to physical and emotional stressors.

Located in dorsal pons. These neurons are implicated in some anxiety symptoms, but they are not serotonergic and not affected by SSRIs.

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40
Q

The nucleus basalis of Meynert houses what type of neurons? What pathology is associated with it?

A

Houses cell bodies of cholinergic neurons.

Alzheimer disease, these neurons secrete DEC amounts of acetylcholine

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41
Q

Where is the red nucleus located and what is it involved in?

A

Located in anterior midbrain

Its neurons participate in motor coordination of upper extremities

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42
Q

The substantia nigra contains what neurotransmitter? Which pathology is associated with it?

A

Contains dopaminergic neurons.

Parkinson disease, these neurons are depleted of dopamine

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43
Q

What is opisthotonos and what is it associated with?

A

Contractions of back muscles resulting in backward arching due to clostridium tetani infection

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44
Q

Vibrio cholera stimulates what release from where that causes the extreme fluid secretion seen in cholera?

A

Serotonin release from enterochromaffin cells in GI tract is stimulated by Vibrio cholera enterotoxin. INC serotonin release contributes to extreme fluid secretion.

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45
Q

What are organophosphates? How do they work? What are the symptoms associated with organophosphate poisoning?

A

Organophosphates are cholinesterase inhibitors. They inhibit breakdown of acetylcholine, leading to cholinergic excess.

Symptoms of organophosphate poisoning include salivation, lacrimation, diaphoresis, bradycardia, and bronchospasm

(refer to picmonic)

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46
Q

How do you treat organophosphate poisoning?

A

Treat using muscarinic antagonists (atropine) and pralidoxime (PAM), a drug that reactivates acetylcholinesterase by binding organophosphates and decoupling them from the enzyme

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47
Q

How does ataxia telangiectasia present clinically?

A

Autosomal recessive resulting from defect in DNA-repair genes. The DNA of patients is hypersensitive to ionizing radiation. Manifests as cerebellar ataxia, oculocutaneous telangiectasias, repeated sinpulmonary infections, and an INC incidence of malignancy.

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48
Q

What are some inherited disorders caused by deficient DNA-repair enzymes? (5)

A

1) Ataxia telangiectasia-characterized by DNA hypersensitivity to ionizing radiation
2) Xeroderma pigmentosum, DNA hypersensitive to UV radiation, causing premature skin aging and INC risk of skin cancer (malignant melanoma and squamous cell carcinoma)
3) Fanconi anemia - caused by hypsersensitivity of DNA to cross-linking agents
4) Bloom syndrome - characterized by generalized chromosomal instability. INC susceptibility to neoplasms too.
5) Hereditary nonpolyposis colorectal cancer (HPNCC) occurs due to defect in DNA mismatch-repair enzymes. Leads to INC susceptibility to colon cancer

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49
Q

Alzheimer disease

A

Neurofibrillary tangles in neocortex

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50
Q

Parkinson disease

A

Loss of neurons in substantia nigra

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51
Q

Huntington disease

A

Atrophy of caudate nucleus

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52
Q

Vit. B12 deficiency and syphillis

A

Posterior column involvement

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53
Q

Parkinsonism

A

Presence of Lewy bodies is characteristic

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54
Q

Alteration of gene expression in Huntington disease occurs how?

A

Hypo-acetylated histones bind tightly to DNA and prevent transcription of genes in their associated regions. Alteration of gene expression in Huntington disease occurs in part due to deactylation of histones. This prevents transcription of certain genes that code for neurotrophic factors, contributing to neuronal cell death.

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55
Q

Acetylating histones normally does what?

A

Weakens the DNA-histone bond and makes DNA segments more accessible for transcription factors and RNA polymerases, enhancing gene transcription.

-In Huntington, abnormal huntingtin gene causes INC histone DEactylation, silencing the genes necessaey for neuronal survival.

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56
Q

Which step of neurotransmission is affected when voltage gated calcium channels are selectively inhibited?

A

Fusion and release of neurotransmitter vesicles

Voltage gated sodium channels are important for generation and propagation of action potentials. When action potential reaches axon terminal, voltage gated calcium channels open and allow influx of calcium, which is essential for fusion and release of neurotransmitter vesicles into the synaptic cleft.

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57
Q

What hypnotic agent is known to have anxiolytic, muscle relaxant, and anticonvulsant actions? Explain its MOA

A

Benzodiazepines INC frequency of opening of the CNS GABAa receptor-chloride channels and have anxiolytic, anticonvulsant, and muscle relaxant effects as well as sedative hypnotic effects.

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58
Q

Pain that WORSENS on inspiration is referred to what? What is indicative of?

A

Inflammation of the pleura

Referred as pleuritic chest pain

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59
Q

What are Kulchitsky cells?

A

Enterochromaffin cells/neuroendocrine cells found throughout conducting zone of tracheobronchial tree. These cells secrete peptide hormones that regulate airway and vascular tone.

Cells of origin for small cell carcinoma of the lung.

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60
Q

What are clara cells?

A

Nonciliated, dome-shaped cells found within airways of conducting zone and respiratory bronchioles. These cells secrete a surfactant like material which coat luminal surface of bronchioles to prevent luminal adhesion so that should they collapse (as they often do), these bronchioles are able to reexpand.

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61
Q

What comprises the conducting zone of the lungs?

A

Conducts air from outside into alveolar-respiratory zone, where gas exchange occurs. NO ACTUAL GAS EXCHANGE OCCURS in conducting zone, thus, it comprises the anatomic DEAD SPACE.

Consists of nose, pharynx, trachea, bronchi, and terminal bronchioles.

Compised of first 16 generations (branches) of respiratory tree. As generation number INC (and airway DEC in size), there is a DEC in amount of mucus-secreting cells, cilia, submucosal glands, and cartilage in airway walls

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62
Q

What comprises the respiratory zone of the lungs?

A

This zone participates in gas exchange. Begins at generation 17 with the respiratory bronchioles and alveolar ducts, terminating blindly as alveolar sacs or acini.

The alveolus is fundamental unit of gas exchange and as generation number INC, an INC number of alveoli are present, culminating in alveolar sacs, which consist solely of alveoli

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63
Q

Tidal volume (TV)

A

amount of air drawn into lungs during normal respiration

normally about 500mL

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64
Q

Inspiratory reserve volume (IRV)

A

Volume of air that can be inhaled during a max inspiration beyond the tidal volume

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65
Q

Expiratory reserve volume (ERV)

A

Volume of air that can be exhaled in a forced expiration beyond the tidal volume

Normally 1,200mL

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66
Q

Residual volume (RV)

A

Amount of air that remains in lungs at end of max respiration. Cannot be measured by spirometry.

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67
Q

Total lung capacity (TLC)

A

TLC = RV + ERV + TV + IRV

Combination of all lung volumes

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68
Q

Vital capacity (VC)

A

Volume that can be exhaled after max inspiration. Includes everything but RV. VC INC with male gender, physical conditioning, and body size, and DEC with age.

VC = ERV + TV + IRV

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69
Q

Functional residual capacity (FRC)

A

Volume remaining in lungs after normal expiration. It is the resting or equilibrium volume of the lungs. B/c it includes RV, cannot be calculated with normal spirometry.

FRC = ERV + RV

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70
Q

Inspiratory capacity (IC)

A

Max volume that can be inspired after a normal expiration

IC = IRV + TV

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71
Q

Explain FEV1/FVC ratio and implications

A

Forced expiratory volume in 1 sec (FEV1): volume of air that can be forcibly expired in one 1 sec after a full inspiration

Forced vital capacity (FVC): volume of air that can be forcibly expired after a full inspiration

FEV1/FVC ratio: is normally about 0.8, means that 80% of VC can be forcibly expired in the 1st second. Obstructive lung disease produces a reduced ratio (0.8).

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72
Q

S1 heart sound

A

Closure of tricuspid and mitral valves. Marks end of diastole because filling of the ventricles is complete.

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73
Q

S2 Heart sound

A

Closure of pulmonic and aortic valves, referred to as P2 and A2 respectively. Marks end of systole b/c ejection of blood from the ventricle has been completed.

During inspiration, intrathoracic pressure becomes more negative, “sucking” more blood back into the right atrium from the vena cava, INC venous return. This INC right ventricular preload, leading to larger right ventricular stroke volume, prolonging duration in which pulmonic valve is open (needs more time to eject all that extra blood). This moves P2 after A2 and causes the S2 sound to be split (physiologic splitting - normal).

On expiration, this does not occur and P2 and A2 occur at same time, causing S2 sound to not be split.

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74
Q

Fixed splitting (heart)

A

When splitting occurs on both inspiration and expiration. Occurs with an atrial septal defect (ASD) b/c there there is a hole between the two atria.

B/c there is a left to right shunt present (b/c left atrial pressures are higher than right atrial pressures), the right ventricle always has INC preload, and the pulmonic valve will always close AFTER the aortic valve.

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75
Q

Wide splitting (heart)

A

When the P2-A2 split is longer than usual, seen with anything that causes a delay in right ventricular emptying. With PULMONIC STENOSIS, the valve is narrowed, and thus takes the blood longer to fully eject, leading to a delay in valve closure.

In right bundle branch block, the fast His-purkinje system to the right ventricle is blocked, and right ventricular contraction is delayed, causing the pulmonic valve to close after the aortic valve b/c the left ventricle will contract and finish ejecting blood first.

76
Q

Paradoxical splitting (heart)

A

When the aortic valve paradoxically closes AFTER the pulmonic valve, seen with anything that causes a delay in left ventricular emptying. This causes the split to paradoxically occur during expiration rather than inspiration. This is due to the pulmonic valve closing earlier than the aortic valve owing to pathology, but during inspiration the INC volume moving thru the pulmonic valve allows the valves to open for the same amount of time. Aortic stenosis and left bundle branch block can cause this, for the same reason described with wide splitting, just now affecting the left ventricle.

77
Q

S3 heart sound

A

Normal in children, abnormal in adults and usually signifies volume overload. When the tricuspid valve and mitral valve open during diastole, the extra volume rushes into the ventricle, tensing the chordae tendineae (tendons that tether the valve to the heart) of the affected valve (depending on which side heart is overloaded with volume), causing the extra sound. This sound is heard during the rapid ventricular filling phase in early diastole and is positioned after the S2 sound.

78
Q

S4 heart sound

A

At the very end of diastole, the atria contract, called the “atrial kick”, to try to squeeze in the last bit of blood before the mitral and tricuspid valves close (S1 sound). If the ventricle is stiff and noncompliat (such as from hypertrophy from hypertension), there will be no room for the extra blood and the S4 sound will be generated. B/c the atrial kick occurs just before the end of diastole and closure of the AV valves, this sound is heard just before the S1 sound.

79
Q

What does a heart murmur/bruit indicate?
Stenosis?
Regurgitation?

A

Blood flow thru heart normally is laminar and silent. When there is TURBULENT blood flow thru the heart, a murmur is heard (turbulent flow thru a narrowed artery is instead called a bruit).

Stenosis is a problem with OPENING a valve, b/c it has been narrowed, whereas regurgitation (or insufficiency) is a problem with keeping a valve closed.

During systole, aortic and pulmonic valve should OPEN to allow for ejection of blood from ventricles, and thus murmur of aortic or pulmonic stenosis will be heard during systole. B/c the tricuspid and mitral valves should be CLOSED, the murmur of tricuspid or mitral regurgitation will also be heard during systole.

80
Q

Aortic or pulmonic stenosis

A

“Crescendo-decrescendo” or “diamond shaped” b/c as the contraction of the heart progresses, the pressure builds up and drops again, leading to a murmur that INC and then DEC in intensity. Pts with aortic stenosis will often complain of chest pain b/c of INC myocardial oxygen demand from the INC afterload. They may also experience exertional syncope b/c the demands for INC CO during exercise can’t be met with the high resistance thru the aortic valve and will experience syncope owing to cerebral hypoperfusion.

Physical exam will show pulsus parvus et tardus, weak (parvus) and late (tardus) pulse.

Predisposing factors to aortic stenosis include congenital bicuspid aortic valve (2 cusps instead of 3) and rheumatic heart disease causing damage to the aortic valve.

81
Q

Mitral or tricuspid regurgitation

A

“Holosystolic” or “pansystolic” b/c it occurs at same intensity for the duration of systole. This is b/c the left and right atria have low pressure and can accept blood even at low pressures if the valve is incompetent.

82
Q

Mitral valve prolapse

A

Most frequent valvular lesion, where an abnormally thickened valve “prolapses” into the left atrium during systole. The sudden tensing of the chordae tendinae that stops the movement of the valve causes a “click” to be heard, and subsequently, a murmur is present. Often a benign lesion.

83
Q

Ventricular septal defect

A

if there is a passage between the left and right ventricles, during systole the left ventricle (which has higher pressures) will eject blood into the right ventricle, leading to a left-to-right shunt. This leads to a holosystolic murmur, similar to that of mitral regurgitation. It is classically described as “harsh” sounding, whereas regurgitant murmurs are “high pitched”.

84
Q

Diastole

A

During diastole, the tricuspid and mitral valves should be open to allow for ventricular filling thru the atria, and thus murmurs of tricuspid or mitral stenosis will be heard during diastole. Conversely, the aortic and pulmonic valves should be closed to prevent backward flow of blood from the arteries into the ventricles, and thus the murmurs of aortic or pulmonic regurgitation will be heard during diastole. In contrast to systolic murmurs, which can be benign, diastolic murmurs are always pathologic.

85
Q

Mitral or tricuspid stenosis

A

The murmur is described as beginning with an opening “snap” when the stenotic valve finally opens, followed by a turbulent rumbling murmur. Most commonly caused by RHEUMATIC fever, which most often affects the MITRAL valve.

86
Q

Aortic or pulmonic regurgitation

A

Early decrescendo b/c after the ventricles eject blood, the valves should shut-failure to do so causes blood to crash back into the ventricle during diastole, leading to the murmur. B/c in aortic regurgitation, the blood crashed back into the left ventricle instead of staying in the systemic circulation, there is a wide pulse pressure from DEC diastolic blood pressure. This drop in diastolic blood pressure leads to many clinical signs, including a large volume pulse that collapses in diastole (Water-hammer pulse); de Musset sign, in which the head bobs with the heartbeat; and Quincke sign, in which the capillary bed in the nail can be seen to be pulsating from the wide pulse pressure.

87
Q

Stable angina (picmonic)

A

http://www.picmonic.com/topics/stable-angina_2030

88
Q

Unstable angina (picmonic)

A

http://www.picmonic.com/topics/unstable-angina_2031

89
Q

Aortic Stenosis (picmonic)

A

http://www.picmonic.com/topics/aortic-stenosis_94

90
Q

Aortic Regurgitation (picmonic)

A

http://www.picmonic.com/topics/aortic-regurgitation_305

91
Q

Tricuspid Regurgitation (picmonic)

A

http://www.picmonic.com/topics/tricuspid-regurgitation_226

92
Q

Mitral Stenosis (picmonic)

A

http://www.picmonic.com/topics/mitral-stenosis_320

93
Q

Mitral Regurgitation (picmonic)

A

http://www.picmonic.com/topics/mitral-regurgitation_138

94
Q

Alpha (type 1) error

A

Rejecting null hypothesis when it is true, creating a “false alarm”.
Think “A” for alarm and type 1 b/c A is first letter of alphabet.

Alpha aka level of significance b/c it is the predetermined level below which the differences are considered unlikely to be due to chance alone and the null hypothesis is rejected. Alpha is usually set at 0.05

Ex: study finds use of vit. C improves recovery from a URI when, in fact, it does not.

95
Q

Beta (type 2) error

A

Failing to reject null hypothesis when it is false, creating a “missed detection”.

Ex: study finds that there is no significant DEC in mortality for patients who regularly exercise, when, in fact, there is.

96
Q

Power (biostats)

A

The ability of a test to reject the null hypothesis when it is false. The probability of avoiding type 2 error.

Power = 1 - beta

Power is INC with INC effect size and INC sample size

97
Q

P-value

A

The probability of obtaining a test statistic (such as a t-test of chi-square test statistic) as extreme or more extreme by chance alone if the null hypothesis is true and there is no bias. A P-value less than 0.05 is usually said to be statistically significant

98
Q

Confidence interval

A

A range of values around the point estimate such that, with repetition, the true value will be contained with a specified probability of 1 - alpha. Most often, the 95% confidence interval is reported, corresponding to an alpha level of 0.05.

INC sample size will narrow CI. A test in which 95% CI contains the “true” value = accurate. A test with a narrow CI is precise.

If 95% CI does NOT contain null result, then there is a statistically significant difference in the groups. Null result depends on the test

For ratios (RR, OR), the null value = 1
For differences, null value = 0
99
Q

Experimental study

A

Investigator controls exposure assignment. Ex: is randomized control trials

100
Q

Observational study

A

Investigator observes the subjects without intervention. Cross-sectional, case-control, and cohort studies are observational studies

101
Q

Cross-sectional study

A

Subjects are enrolled without regard to exposure and disease status, which are then evaluated simultaneously. Most often a survey. Designed to determine number of people with disease at a given time is a prevalence study.

Ex: How many people in US have AIDS?
Ex 2: How many people with hyperlipidemia also currently have coronary artery disease?

102
Q

Case-control study

A

Subjects are enrolled based on disease status, one group with disease (cases), and one group without (controls), and then exposure is assessed in the 2 groups. Case control are retrospective where disease status is known before exposure assessment.

Ex: Select subjects with and without mesothelioma then ascertain the proportion of each group previously exposed to asbestos

103
Q

Cohort study

A

Subjects are enrolled based on exposure status, one cohort with the exposure and one without (controls), and followed over time for the disease of interest. Subjects must be free of the disease at enrollment. Study may be prospective (disease status not known at time of enrollment) or retrospective (chart review). Incidence in each group can be calculated. Relative risks are calculated for effect measure estimation.

Ex: does having elevated cholesterol INC your chance of having a MI?

  • Prospective design: Patients with and without high cholesterol are enrolled and followed over time to see if they develop heart disease
  • Retrospective: Patients with and without high cholesterol are identified from 10-yr old hospital records. Their charts are then reviewed thru the present date to determine whether they developed heart disease.
104
Q

Crossover study

A

A type of prospective study, usually RCT (randomized control trial) but possibly a cohort study, in which each patient begins in either the control or treatment group and then crosses over to the other group. This way, every patient serves as his or her own control.

Ex: Pts randomly assigned either placebo or a tricyclic antidepressant to treat their fibromyalgia. After period of time receiving one treatment, the group switch to see if the placebo group improves on medication.

105
Q

Meta-analysis

A

A study that pools results of several similar studies to INC statistical power by INC overall study size. If individual studies are of high quality, a meta-analysis can produce the most convincing level of evidence. However, a meta-analysis cannot compensate for poor research -“garbage in equals garbage out.”

106
Q

Clinical trials (phase 1)

A

First stage of testing in human subjects. Small group of HEALTHY volunteers given a medication to determine safety, pharmacodynamics, and pharmacokinetics of the medication.

107
Q

Clinical trials (phase 2)

A

In this stage, a slightly larger group of patients with the target condition is given the drug to determine EFFICACY, OPTIMAL DOSING, and SIDE EFFECTS. Many drugs fail in phase 2 b/c they are determined not to work as planned.

108
Q

Clinical trials (phase 3)

A

Large randomized controlled trials to determine efficacy of a drug compared with placebo or a “gold standard”. Phase 3 trials must prove both SAFETY and EFFICACY. of a drug for it to be approved by the US Food and Drug Administration (FDA).

109
Q

Confounding bias

A

Another variable related to both exposure and outcome, is unevenly distributed between groups and distorts the association of interest

Ex: Study finds that drinking coffee is associated with lung cancer b/c the study fails to recognize that coffee drinkers are also more likely to be smokers

Solution: Matching is one solution, which distributes confounders evenly between groups.

110
Q

Selection bias

A

Groups are not similar at baseline b/c of non-random assignment

Sampling bias (ascertainment bias): A sample is selected that does not accurately represent the population it is intended to. These studies may have INTERNAL validity (accurate within the study), but lack EXTERNAL validity (results are not generalizable to the population as a whole.

Ex: A study inadvertently selects members of a lower socioeconomic class by offering a small financial compensation for a study

Ex2: A study to examine heart disease does not have any patients over 65 yrs of age. The study may have INTERNAL validity, but lacks EXTERNAL validity and cannot be extrapolated to the general population (in which most patients with heart disease would be older than 65 yrs).

Solution: Random sampling

111
Q

Susceptibility bias

A

Patients who are sicker are selected for a more invasive treatment

Ex: Sicker pts get selected for surgical management over medical management of heart disease. Studies then show medical management to be associated with better outcomes simply b/c pts were healthier at baseline.

Solution: Randomization

112
Q

Attrition bias

A

If LOSS to FOLLOW-UP is unequal between the intervention and control groups, it can make an intervention seem more effective than it is.

Ex: New acne medication may work for some pts, but causes unwanted side effects. Many pts who are taking the medication and have unimproved acne drop out of the trial, compared with those taking placebo. The medication appears to have cured acne much more consistently than in reality b/c the unimproved pts dropped out.

Solution: Gather as much data as possible from dropouts.

113
Q

Measurement bias (Hawthorne effect):

A

People change their behaviors when in a study.

Ex: Participants in a medication trial to treat hypertension more likely to adopt a healthy lifestyle if they know they are being studied. A DEC in BP then occurs b/c of lifestyle changes but is attributed to the medication.

Solution: Use a placebo group

114
Q

Recall bias

A

Pts’ recall of an exposure may be affected by their knowledge of their current disorder

Ex: Nonsmoker with lung cancer reports significant exposure to 2nd-hand smoke as a child. On other hand, a healthy nonsmoker with the same degree of exposure forgot all about his uncle who smoked indoors.

Solution: Search for confirmatory or objective sources of info or conduct a prospective study.

115
Q

Lead-time bias

A

Detecting a disease earlier may be misinterpreted as improving survival.

Solution: Scrutinize any screening study for lead time bias and ask, “Is this actually improving survival or only detection?” Adjust survival rates according to severity of disease (i.e. survival from stage T1, N0, M0 prostate cancer, rather than survival from date of detection.

116
Q

Late-look bias

A

Info is gathered too late to make useful conclusions b/c subjects with severe disease may be incapable of responding or deceased.

Ex: Survey of pts with pancreatic cancer reveals only minimal symptoms b/c those with severe disease are too sick to respond or may be deceased.

Solution: Stratify by severity

117
Q

Procedure bias

A

Subjects are treated differently depending on their arm of the study

Ex: Pts assigned to a surgical intervention arm of a study are followed more closely than those assigned to no intervention

Solution: Perform a double blind study to prevent researchers from treating groups differently

118
Q

Experimenter expectancy (Pygmalion effect)

A

The hopes of the experimenter influence the outcome of a study

Ex: A physician hoping to treat fibromyalgia conveys to a patient in the treatment arm his expectations that the medication will work

Solution: Perform a double-blind study to prevent researchers and subjects from knowing to which arm of the study they have been assigned.

119
Q

Informed consent (BRAIN)

A

Requires a discussion with pt that includes the procedural information from BRAIN: Benefits, Risks, Alternatives, Indications for the procedure, and Nature of the procedure.

120
Q

Health maintenance organization (HMO)

A

A type of managed care organization with integration of payment and delivery of health care, in which a group of providers contract with the insurance agency to provide complete care for a patient in exchange for a referral base. All care is coordinated by a primary care provider (PCP), who refers the pt to specialists as necessary.

121
Q

Preferred provider organization (PPO)

A

A type of insurance in which the insurer develops a network of physicians to provide care to their clients at a reduced rate. In exchange, physicians receive access to a population of potential patients. In contrast to an HMO, pts may seek care from any PPO provider, including specialists without a PCP referral.

122
Q

Medicare

A

Federal health insurance plan for those 65 yrs and older and people with certain disabilities. All qualifying citizens receive Part A but must opt in for parts B and D

Part A: In-patient care
Part B: Outpatient care
Part D: Prescription drug coverage

123
Q

Medicaid

A

Joint state and federal program that provides health insurance to impoverished citizens and permanent residents. Qualifications and benefits depend on the state

124
Q

Physician reimbursement: Fee for service

A

Each procedure is reimbursed to the physician. Pitfall: A financial incentive exists for physicians to OVERTREAT patients

125
Q

Physician reimbursement: Capitation

A

A physician is paid a fixed amt for each pt, usually on a monthly basis, regardless of time spent or treatment rendered. Pitfall: Physicians may select for healthier pts or be less likely to order tests

126
Q

Physician reimbursement: Salary

A

Hospitals or HMOs pay a fixed salary to the physician regardless of procedures performed, tests ordered, or number of pts cared for. Pitfall: Physicians may have less productivity

127
Q

Malpractice

A

A physician is at risk for a civil suit if the situation fits the 4 D’s: If the physician has a DUTY to the patient, is DERELICT in the pt’s care, and DIRECTLY causes DAMAGE to the pt.

Malpractice: Dereliction of a physician’s duty that directly causes damage.

128
Q

Starling forces

A

Pnet = (forces promoting fluid leaving capillary) - (forces promoting fluid returning to capillary)

Pnet = [(Pc + PIEi) - (Pi + PIEc)]
Positive Pnet: fluids leave capillary
Negative Pnet: fluids return to capillary

Pc: hydrostatic pressure in capillaries - attempts to push fluid out of the capillary
PIEi: interstitial oncotic pressure-attempts to pull fluid out of the capillary
Pi: hydrostatic pressure in interstitium-attempts to push fluid back into the capillary
PIEc: capillary oncotic pressure-attempts to pull fluid out of the interstitium

129
Q

Murmur summary (step 1 pearl)

A

Left sided lesions much more likely to be tested. Right sided murmurs will usually have a question stem that hints at intravenous drug use (tricuspid regurgitation). Mitral stenosis will often have a question stem that hints at rheumatic fever. Aortic regurgitation will usually be your diastolic murmur without other clues. Main goal will be distinguishing the 2 left-sided systolic murmurs: aortic stenosis (crescendo-decrescendo, radiates to carotids) and mitral regurgitation (holosystolic, radiates to axilla).

130
Q

Left heart failure

A

Disease of SYMPTOMS b/c the symptoms of dyspnea, paroxysmal nocturnal dyspnea (PND), and orthopnea are prominent.

131
Q

Right heart failure

A

Disease of SIGNS b/c peripheral edema, jugular venous distention, and hepatomegaly are prominent.

132
Q

Bibasilar inspiratory crackles are a sign of what?

A

Pulmonary edema (could be a symptom of left heart failure) - transudation of fluid into alveoli due to INC hydrostatic pressure in the pulmonary capillaries b/c the left heart can no longer pump that fluid out. Causes bibasilar inspiratory crackles, b/c inspiration forces air into fluid-filled alveoli that are edematous. Often, there are small hemorrhages, which is why patients with pulmonary edema often cough up a pink frothy liquid. Macrophages eat the blood hemorrhaged into the alveoli but retain the hemosiderin; microscopically, these hemosiderin-laden macrophages = heart-failure cells.

133
Q

What is incidence? Know the formula

A

Incidence of a disease is the number of new cases of a diseases per year divided by the total population at risk.

134
Q

Chlorpheniramine MOA and what other medications should be AVOIDED when prescribed?

A

First generation H1 histamine receptor antagonist (including diphenhydramine) can cause significant sedation, especially when used with other medications that cause CNS depression (such as benzos)

135
Q

Beck’s triad

A

A constellation of three findings in cardiac tamponade:

1) Hypotension from DEC cardiac output
2) Jugular venous distention from blood backing up into the veins b/c the heart cannot fill
3) Muffled heart sounds b/c the heart is being strangled with fluid

136
Q

What is difference between constrictive pericarditis and cardiac tamponade?

A

Constrictive pericarditis: the inflammation can lead to scarring, where the 2 pericardial layers adhere to each other and fill with fibrous tissue, preventing filling of the heart.

Cardiac tamponade: Life threatening emergency. Heart becomes compressed by fluid in the pericardium, preventing filling of the ventricles and subsequently DEC cardiac output. Can be secondary to effusion or bleeding due to trauma (knife thru heart), ventricular wall rupture, or extension of an aortic dissection into the heart

137
Q

Vasopressor effects on alpha1 receptor, beta1 receptor, and beta2 receptor

A

Vasopressors INC systemic vascular resistance by clamping down blood vessels; essentially “antihypotensive agents”.

Alpha1 receptor activity: INC systemic vascular resistance and thus INC blood pressure

Beta1 receptor activity: INC cardiac output thru INC inotropy (contractility) and chronotropy (rate)

Beta 2 receptor activity: Cause vasodilation, DEC systemic vascular resistance, and thus DEC blood pressure

138
Q

Hydralazine

A

Potent arteriole vasodilator. First line treatment for hypertension in pregnancy. Produces significant reflex tachycardia (vasodilates arterioles) so should be administered with a beta-blocker such as labetalol to prevent reflex response. Hydralazine can be used to quickly lower an elevated BP in the peripartum setting as its effect is rapid.

139
Q

Norepinephrine

A

http://www.picmonic.com/learn/norepinephrine_1216

140
Q

Dexamethasone suppression test

A

A low dose of dexamethasone (cortisol analogue) is given and a high dose is given to see if NEGATIVE FEEDBACK is still active to some extent.

Used to distinguish pituitary and ectopic Cushing syndrome.

In low dose, neither pituitary nor ectopic Cushing syndrome will show a DEC in cortisol production.

High dose can differentiate the two, the pituitary still has some negative feedback ability (b/c it is used to having negative feedback) and will show cortisol suppression with high-dose dexamethasone. B/c the ectopic ACTH secreting tumor does NOT have a negative feedback loop, it shows no suppression with either low or high dose.

141
Q

Differentiate primary hyperaldosteronism and secondary hyperaldosteronism

A

In primary hyperaldosteronism, the aldosterone is being secreted INDEPENDENT of RENIN and thus renin levels will be LOW.

Secondary, renin levels will be HIGH

142
Q

Function of chief cells

A

Chief cells are small, round, eosinophilic cells that create parathyroid hormone which is stored until stimulated for release (CCCChief cells have a role in CCCCalcium)

143
Q

Primary hypoparathyroidism

A

Calcium is low and parathyroid gland is not attempting to fix it (low PTH)

144
Q

Hypoalbuminemia

A

DEC albumin leads to DEC total calcium but ionized (free) calcium is normal, and thus PTH is normal range.

145
Q

Secondary hyperparathyroidism

A

High PTH is unable to correct calcium; this can be seen in renal failure b/c vitamin D cannot be made to help correct Ca2+. Note that this could also represent pseudohypoparathyroidism

146
Q

Respiratory alkalosis (in response to calcium levels)

A

Total calcium is normal, but alkalosis causes INC binding of calcium to albumin, leading to DEC ionized calcium and subsequent INC PTH level to INC ionized calcium.

147
Q

Primary hyperparathyroidism

A

High calcium, yet PTH is still high

148
Q

Hypercalcemia of malignancy

A

High calcium, PTH low b/c PTHrP is being created instead (or direct osteolytic bone metastasis)

149
Q

Draw and label brachial plexus

A

MARMU

“Robert Trunk Drinks Cold Beers”

Pg 412 in crush

150
Q

What nerve is involved: Midshaft humeral fracture; axillary compression

  • Nerve roots?
  • Sensory loss?
  • Motor loss?
A

Radial nerve

  • Nerve roots: C5-T1
  • Sensory loss: Dorsum of hand (except 5th and lateral 4th digit)
  • Motor loss: Triceps brachii, extensor carpi radialis
  • Wrist drop: inability to extend wrist
151
Q

What nerve is involved: Distal humeral fracture; carpal tunnel syndrome

  • Nerve roots?
  • Sensory loss?
  • Motor loss?
A

Median nerve

  • Nerve roots: C8-T1
  • Sensory loss: Palmer surface of hand; 1st, 2nd, and 3rd digits
  • Motor loss: Forearm flexors, opponens pollicis, lateral lumbricals
  • Ape hand: nonopposable thumb
152
Q

What nerve is involved: Distal humeral fracture; wrist (hamate) fracture

  • Nerve roots?
  • Sensory loss?
  • Motor loss?
A

Ulnar nerve

  • Nerve roots: C8-T1
  • Sensory loss: 5th digit; lateral 4th digit
  • Motor loss: Wrist finger flexors, intrinsic muscles of the hand
  • Ulnar claw (Pope’s blessing): flexion of 4th and 5th digits
153
Q

What nerve is involved: Proximal humeral fracture; shoulder dislocation

  • Nerve roots?
  • Sensory loss?
  • Motor loss?
A
  • Axiallary nerve
  • Nerve roots: C5-C6
  • Sensory loss: Shoulder (over deltoid muscle)
  • Motor loss: Deltoid, teres minor
  • Inability to ABduct shoulder
154
Q

What nerve is involved: Shoulder dystocia

  • Nerve roots?
  • Sensory loss?
  • Motor loss?
A
  • Upper brachial plexus
  • Nerve roots: C5-C6
  • Sensory loss:
  • Motor loss: Deltoid, infraspinatus, biceps brachii
  • Waiter’s tip: inability to abduct shoulder, externally rotate, or supinate arm
155
Q

What nerve is involved: Traction on raised arm (i.e. during birth or falling from tree)

  • Nerve roots?
  • Sensory loss?
  • Motor loss?
A
  • Lower brachial plexus
  • Nerve roots: C8-T1
  • Sensory loss:
  • Motor loss: Finger extensors, lumbricals
  • Klumpke palsy: total clawing of hand
156
Q

Musculocutaneous nerve

A

Nerve roots: C5-C7

  • Innervates biceps brachii and brachialis muscle, which are responsible for elbow flexion and supination
  • Injury can result from forced stretching between the shoulder and head, damaging the upper trunk
157
Q

What is portal hypertension?

A

Portal hypertension occurs when blood can’t flow properly through the liver, so it backs up behind the liver and causes all kinds of nasty complications, including: ascites, splenomegaly, hepatic encephalopathy, and the formation of portosystemic venous shunts (especially within the rectum and esophagogastric junction).
There are three types of things that can cause portal hypertension: things that prevent blood from getting into the liver (prehepatic causes), things that impair blood flow within the liver itself (intrahepatic causes), and things that block the flow of blood out of the liver (posthepatic causes).

158
Q

What are some prehepatic causes of portal hypertension? (3)

A
  • Obstructive thrombosis
  • Narrowing of portal vein
  • Massive splenomegaly (with increased splenic vein blood flow)
159
Q

What are some intrahepatic causes of portal hypertension? (5)

A
  • Cirrhosis (most cases)
  • Schistosomiasis
  • Massive fatty change
  • Diffuse granulomatous disease (like sarcoidosis)
  • Diseases affecting the portal microcirculation (like nodular regenerative hyperplasia)
160
Q

What are some posthepatic causes of portal hypertension? (3)

A
  • Severe right-sided heart failure
  • Constrictive pericarditis
  • Hepatic vein outflow obstruction
161
Q

What is the difference between delirium and dementia?

A

Delirium is reversible, acute-onset confusional state characterized by a fluctuating level of consciousness with deficits in attention, memory, and executive functions.

Dementia is of GRADUAL onset, is irreversible, and doesn’t involve fluctuations in consciousness.

162
Q

What part of the brain is affected in Huntington’s disease and where is it located?

A

The head of the caudate lies in the inferolateral wall of the anterior horn of the lateral ventricle. It is separated from the globus pallidus and putamen by the internal capsule. The caudate is atrophied in Huntington’s disease.

163
Q

What is the function of the internal capsule and what is its function?

A

The posterior limb of the internal capsule separates the globus pallidus and putamen from the thalamus and carries corticospinal motor and somatic sensory fibers as well as visual and auditory fibers. (Function of this limb is most important to know for USMLE). The genu, or “knee”, of the internal capsule lies between the anterior and posterior branches and carries corticobulbar fibers. The anterior limb of internal capsule separates the caudate nucleus from globus pallidus and putamen and carries a portion of the thalamocortical fibers.

164
Q

What is the function of the insula/insular cortex?

A

The insula plays a role in the limbic system (emotion) as well as in the coordination of some autonomic functions, particularly of the cardiac system.

165
Q

Which drug may precipitate opioid withdrawal symptoms if used on a patient currently taking opioids?

A

Buprenorphine - is a partial opioid receptor agonist that binds with high affinity (potency) and can prevent binding of other opioid medications but has low intrinsic activity (efficacy) for opioid mu-receptors. In patients on long-term opioid therapy, buprenorphine can displace other opioids and precipitate withdrawal. It acts as an opioid receptor antagonist in the presence of full opioid agonists which leads to withdrawal in opioid tolerant patients with chronic pain.

166
Q

How do opioids work? MOA?

A

Opioids work by selectively binding to G protein coupled opioid receptors, mimicking actions of endogenous opioid peptides. BUT, long-term activation of mu-opioid receptors on nociception-transmitting neurons is associated with INC pain sensitivity (central sensitization) due to: 1) INC turnover of inhibitory opioid receptors (receptor downregulation) and decoupling of receptors from their 2nd messenger system (receptor decoupling) and 2) Upregulation of excitatory N-methyl-D-aspartate (NMDA) receptors.

This manifests as an INC dose requirement to provide same level of pain relief (tolerance) and pain sensations triggered by benign stimuli (opioid-induced hyperalgesia).

167
Q

What are the side effects of tricyclic antidepressants (TCAs) such as amitryptyline?

A

TCAs have strong anticholinergic properties that can lead to confusion, constipation, and acute urinary retention. Elderly patients are at INC risk for side effects due to comorbid conditions (dementia, BPH), DEC hepatic and renal clearance of medications, and a higher burden of concurrent medications.

168
Q

Don’t cut the INFUNDIBULOPELVIC ligament, CARDINAL ligament, or URETER or your patient will end up in the ICU

A

pg. 558-559 Crush for diagram

169
Q

Infundibulopelvic ligament

A

AKA suspensory ligament of ovaries. Connects ovaries to pelvic wall and contains the OVARIAN blood vessels

170
Q

Ovarian ligament

A

Connects ovaries to lateral surface of the uterus. Doesn’t contain any vessels

171
Q

Round ligament

A

Connects uterine fundus to the labia majora by passing thru the deep inguinal ring. Round ligament is a derivative of the embryologic gubernaculum.

172
Q

Cardinal ligament

A

Connects the cervix to the pelvic side wall. It contains the UTERINE blood vessels

173
Q

Broad ligament

A

Connects the ovaries, fallopian tubes, and uterus to the pelvic floor and side wall.

174
Q

Pouch of Douglas

A

The anatomic space between the rectum and uterus. It can be palpated via a digital rectal exam. It is important b/c it can be a collecting site of blood (from ruptured ectopic pregnancy), pus (from pelvic inflammatory disease), malignant cells (from ovarian cancer), or endometrial implants (from endometriosis).

175
Q

Which side of the body are varicoceles more common?

A

Varicoceles are more common on the left side b/c the left testicular vein drains into the left renal vein before the inferior vena cava.

176
Q

Where do the ovaries and testes drain into lymphatically?

A

Para-aortic nodes b/c the ovaries and testes descended from the abdomen with their blood source from the aorta.

177
Q

Where do the scrotum and distal third of the vagina drain into lymphatically?

A

Superficial inguinal nodes.

178
Q

Where do the uterus and proximal 2/3rds of the vagina drain into lymphatically?

A

External iliac, obturator, and hypogastric nodes

179
Q

In males, how is spermatogenesis maintained?

A

Lh stimulates Leydig cells to secrete testosterone. fSh stimulates Sertoli cells (Support cells) to maintain spermatogenesis.

180
Q

Mnemonic: During reproductive years, there are 2 (husband and wife) in the house - estraDIol. During pregnancy, there are 3 (husband, wife, child) - esTRIol. During menopause, sadly u might be a widow: estrONE.

A
  • Estradiol = most potent estrogen. Produced by ovary and most abundant estrogen in premenopausal women.
  • Estrone is less potent and adipose tissues produces it by aromitization of androstenedione (released from the adrenal cortex and gonads).
  • Estrone production doesn’t require ovaries and is the most abundant estrogen in postmenopausal females and males.
  • Estriol is least potent estrogen and only present in significant levels during pregnancy. The placenta produces estriol by aromitization of fetal androgens. Can be used as marker for fetal well being.
181
Q

Sertoli cells Support what?

A

Spematogenesis. They secrete ABP (androgen-binding protein) which maintains a high testosterone level in the seminiferous tubules; inhibin which provides negative feedback and inhibits FSH secretion that normally would stimulate sertoli cells; Mullerian inhibiting hormone, which during fetal development inhibits the default female mullerian system from developing.

182
Q

What is the function of human placental lactogen?

A

Produced by synctiotrophoblasts of the placenta. DEC maternal insulin sensitivity and thus raises maternal serum glucose levels. Maintaining adequate glucose is crucial to fetal development. Can be the cause of gestational diabetes.

183
Q

What are the clinical signs of ectopic pregnancy?

A

Vaginal bleeding (minimal to moderate), pelvic pain, and adnexal mass

184
Q

Painless 3rd trimester bleeding is what?

Painful 3rd trimester bleeding is what?

A

Placenta previa is when placent attaches to lower uterine segment and partially covers the cervix. Causes PAINLESS vaginal bleeding.

Placenta abruption is premature separation of the placenta, causing PAINFUL vaginal bleeding, fetal distress, and tetanic (constant maximal) contractions.

185
Q

Enteral absorption

A

Absorbed thru the intestines: oral and rectal

186
Q

Parenteral absorption

A

Absorbed withOUT the intestines: IV (intravenous), IM (intramuscular), SQ (subcutaneous), inhaled, topical, or transdermal