Lab exam 1 Flashcards

1
Q

what is a lobotomy? describe procedure

A

use electroconvulsion to make the patient unconscious (later was done on conscious patients). Insert an ice pick up through the eye orbital by tapping with hammer. Pick breaks through the soul into the frontal lobe. Wiggle the pick back and forth to scramble the frontal lobe.

Results: calms emotions, demobilizes the person, lack of social life, child-like uninhibited behavior, basically completely lost themselves

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2
Q

what circumstances allowed lobotomies to gain popularity

A

There was a large mental illness problem and no solution offered. hospitals were overcrowded and had terrible conditions for mentally ill people. After the war, veterans came back and the problem got even worse. People would accept wild ideas to solve this problem, and lobotomies had somewhat successful results initially, although terrible long term effects. Doctors delivering public criticism wasn’t really a thing at the time so they couldn’t stop it from spreading in popularity. The press was a big fan of the operation because it was a “miracle surgery” and Freeman was happy to make it a spectacle for them.

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3
Q

Who invented lobotomies? name all of the important players in the development

A

Egas Moniz: won Nobel prize for his operation of altering the frontal lobe to solve mental illness
Walter Jackson Freeman: inspired by Moniz, came up with the idea of frontal lobe surgery that would evolve into the lobotomy
James Watts: worked with Freeman and assisted with the initial surgeries. Left Freeman after seeing his simplified lobotomy where an ice pick is hammered through the eye.

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4
Q

Chemical lobotomies are possible by what drug

A

Thorazine

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5
Q

define leukemia and the types of leukemia

A

Leukemia is a blood/bone marrow cancer that causes increased white blood cells

Acute Lymphoblastic leukemia (ALL): rapid increase of immature blood cells, crowding the marrow and stopping production of healthy blood cells. Cancerous change takes place in precursors to lymphocytes, often B cells

Chronic Lymphoblastic leukemia (CLL): excessive build up of mature (abnormal) white blood cells. Cancerous change takes place in precursors to lymphocytes, often B cells (Hairy cell leukemia is a subtype of CLL, uncommon, characterized by abnormal B lymphocytes)

Acute Myelogenous leukemia (AML): rapid increase of immature blood cells, crowding the marrow and stopping production of healthy blood cells. Cancerous change takes place in precursors to red blood cells, other white blood cells, and platelets

Chronic Myelogenous leukemia (CML): excessive build up of mature (abnormal) white blood cells. Cancerous change takes place in precursors to red blood cells, other white blood cells, and platelets

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6
Q

what demographics are most often affected by each type of leukemia

A

Acute lymphoblastic leukemia (ALL): most common in children. Also some older adults
Chronic lymphoblastic leukemia (CLL): older adults over 55, sometimes younger adults. Never children. two thirds of affected people are men.
Acute myelogenous leukemia (AML): more in adults than children, more in men than women
Chronic myelogenous leukemia (CML): mainly adults, very small number of children

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7
Q

Common symptoms of leukemia

A

easily bruised, bleed excessively, develop pinprick bleeds called Petechiae, weak immune system, anemia, dyspnea, pallora

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8
Q

how is leukemia diagnosed

A

count blood cells under microscope and perform bone marrow examination. A high number of white blood cells are apparent under microscope when leukemia is present. A lymph node biopsy may also be helpful to diagnose

Sometimes there is not a high white blood cell count in the bloodstream, this is called aleukemia. The bone marrow still contains cancerous white blood cells but they stay in the marrow so aren’t seen in the blood test.

**The Avier Rod is an indicator of AML

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9
Q

known causes of leukemia

A

ionizing radiation
viruses like Human T-lymphotropic virus (for adult T cell leukemia)
Benzene and alkylating chemotherapy agents
Tobacco use (for AML in adults)
petrochemicals
hair dyes
maybe high ELF magnetic fields

there is also some genetic predisposition, people with Down syndrome are high risk.

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10
Q

name the types of white blood cells in order from most common to least common

A

Neutrophils, lymphocytes, monocytes, eosinophils, basophils (never let monkeys eat bananas)

blood cells that are not WBCs are erythrocytes (RBCs) and platelets

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11
Q

Identify what each leukemia type looks like under microscope

A

ALL: lots of immature lymphocyte precursors with larger nuclei.
CLL: lots of mature appearing lymphocytes, often the blood smear ruptures the lymphocytes and they appear as “smudge cells”
Hairy cell leukemia: lots of B cell lymphocytes that look hairy
AML: lots of immature myeloblasts with prominent nucleoli. Auer rods (eosinophilic rod-like cytoplasmic inclusions) are helpful to identify AML with.
CML: lots of basophils and eosinophils and more immature myeloid cells. Not as many blasts as AML

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12
Q

What did the guy in the vital signs “watermelon” article have? how did they treat?

A

Chronic myelogenous leukemia. Treated by Gleevec, a drug that inhibits the mutant tyrosine kinase produced in patients which causes the uncontrolled multiplication of white blood cells.

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13
Q

describe the action of a monosynaptic stretch reflex

A

Tendon is stimulated (like by reflex hammer), sensory spindle detects stimulus and sends input to the spinal cord, information crosses one synapse to a motor neuron that sends output and causes muscle to contract.

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14
Q

describe the action of a polysynaptic reflex

A

tendon is stimulated, sensory neuron sends signals ALSO to interneurons in the spinal cord which connect and signal other motor neurons, these send output and cause antagonistic muscles (like hamstrings) to relax (extend?) while agonist muscle contracts

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15
Q

describe deep tendon reflexes

A

DTR’s flex muscles back to normal position. Sensory input from fully contracted muscle is sent to spinal cord, which signals the two groups of muscles via interneurons. One signal tells the contracted muscle (like the quads) to relax and the other signal tells the relaxed muscle (like the hamstrings) to contract. Returning to resting position (in this example the calf is resting)

DTRs oppose stretch reflexes!

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16
Q

what is the “step on a tack” reflex

A

You step on a tack and the stimulus is sent to the spinal cord and distributed to multiple regions. Output is sent to the side where pain is felt and to the opposite side, telling the non-injured side to extend and the injured side to flex off the tack. This results in a hop

17
Q

achilles tendon reflex

A

percuss the achilles tendon = foot plantar flexes. exaggerated with upper motor neuron damage, absent in lower motor neuron damage

18
Q

babinski’s reflex

A

downward curling of toe 1 following lateral stroking of the sole from heel to base of toes. If the toe extends and outer toes flare, this shows pyramidal tract lesions. Also normally like that in infants <6 months

19
Q

Biceps reflex

A

percuss biceps branch insertion tendon = forearm flexes

20
Q

ciliospinal reflex

A

stroke/scratcj=h/pinch the skin of the back of the neck = pupillary dilation

21
Q

knee jerk reflex

A

percuss the patellar ligament = lower leg extends. Absent in lower motor neuron damage, exaggerated in upper motor damage

22
Q

light reflex

A

pupil constricts with light shone on it

23
Q

moro startle reflex

A

(infants) blow in face/on top of abdomen = rapid abduction/extension of arms (hugging). disappears after 1-2 months, absent also if brain damage or birth-originated injury occurs

24
Q

piliomotor reflex

A

goose flesh due to skin cooling rapidly or emotional reaction

25
Q

corneal reflex

A

eyelids close due to corneal irritation

26
Q

cremasteric reflex

A

stroke front of inner thigh = testicular retraction

27
Q

triceps reflex

A

percuss triceps insertion tendon = forearm extension while arm is held loosely bent position

28
Q

palmar grasp reflex

A

lightly stroke the palm = grasps at stimulus, present from birth to 6 months

29
Q

red light reflex

A

reflected red light on ophthalmological exam indicates lack of cateracts

30
Q

rooting reflex

A

stroke cheek = moth moves to stimulus, present from birth to 4 months (awake) or 7 months (asleep)

31
Q

babinski’s SIGN

A

decreased or absent achilles tendon reflex in sciatica

32
Q

Perez reflex

A

hold baby face down and apply suprapubic pressure, stroke paraspinous muscles and hold container beneath genitals = baby cries, back extends, legs/arms reflection occurs, baby urinates

33
Q

Type I vs type II muscle fibers

A

type I: slow twitch fibers, primarily aerobic, good endurance, lots of mitochondria and myoglobin. have many small capillaries and small motor units

type II: fast twitch fibers, primarily anaerobic, fatigue easily, few mitochondria and myoglobin. Have few capillaries with larger diameter and require stronger stimulus

34
Q

define motor unit, motor unit summation, and wave/temporal summation

A

motor unit: a somatic motor neuron and all of the muscle fibers in innervates

summation: recruitment of motor units, some with higher stimuli thresholds, to regulate strength of contraction. result of increased STRENGTH of stimulation

wave/temporal summation: series of contractions built on each other. the opportunity for relaxation between contractions decreases with more frequent stimuli until a point is reached where the muscle cannot relax between stimuli and a sustained contraction or TETANUS is reached. this is due to the increased FREQUENCY of stimulation

35
Q

what causes muscle fatigue

A

in anaerobic respiration, muscles produce lactic acid (lactate) while in aerobic they produce CO2 and H2O. Lactic acid accumulates in the muscle and drops pH, causing enzymes in fibers to reduce activity, so causing fatigue. this causes only short term fatigue as the lactic acid is removed from the muscle and converted back to glucose via gluconeogenesis. Adequate circulation is essential for removal of lactic acid. Long term fatigue can be caused by depletion of glycogen