Med Surg Quiz 3 Evans

Front 1

What hemisphere of the brain is the most dominant?

Back 1

The Left Hemisphere

Front 2

What hemisphere is considered to deal with creativity?

Back 2

The Right Hemisphere

Front 3

What is the diencephalon of the brain?

Back 3

It is the structure that lies under the cerebrum and contains the thalamus and hypothalamus.

Front 4

What is the thalamus responsible for?

Back 4

crude sensation except smell

Front 5

What is the hypothalamus for?

Back 5

produces triggering signal hormones for the pituitary gland

Front 6

What is hypophysis?

Back 6

A technical term for pituitary.

Front 7

What is the pituitary?

Back 7

master gland of the body that regulates multiple functions

Front 8

What is the brainstem?

Back 8

(dinosaur brain) that controls basic funcion such as sleep, wake, and response to noxious (harmful, unpleasant, poisonous) stimuli. Also controls temperature and respirations

Front 9

What does the cerebellum do?

Back 9

Coordinates fine motor movement
controls voluntary actions
gauges distance and speed

Front 10

Sensory receptors interact with what nerves?

Back 10

the afferent nerves

Front 11

Lower motor neurons interact with what neurons?

Back 11

The efferent neurons

Front 12

The sympathetic nervous system is located ?

Back 12

between T1 and L2-L3. Provides fight or flight

Front 13

The parasympathetic NS is located?

Back 13

between S2-S4 and cranial nerves III, VII, IX, and X

Front 14

Signs of ALOC are?

Back 14

Confusion
Drowsiness
Lethargy
Headache
Visual disturbances

Front 15

Signs of a stroke are?

Back 15

Ataxic (jerky) gait
Muscle weakness
Slurred Speech
Unilateral loss of motor fxn
sudden loss of bowel and/or bladder control
sudden lower extremity weakness

Front 16

Migraine

Back 16

episodic manifested by frontotemperal, throbbing pain often worse behind one eye or ear. Often accompanied by sensitive scalp, anorexia, photophobia, and nausea, with or without vomiting.

Front 17

Cluster Headaces

Back 17

Unilateral, culotemperal or oculofrontal headache with boring, excrutiating, and nonthrobbing. Pain may radiate. Usually accompanied by ipsilateral tearing of eye, rhinorrhea, ptosis, and miosis.

Front 18

Tension headache

Back 18

Characterized by back and shoulder muslce tenderness and bilateral pain in the base of the skull and on the forehead. Appears to be related to stress.

Front 19

Signs of a stroke are?

Back 19

Transcient or prolonged loss of consciousness, lethargy or drowsiness. Difficulty with focusing on tasks. Blurred vission, unilateral numbness of face and extremities, loss of proprioception, dysphasia, aphasia, neglect syndrome, hemiplegia (paralysis), hemiparesis (weakness), hypotonia (dec. muscle tone) or hypertonia (muscles are flexing), hypoglossia.

Front 20

Alzheimer's

Back 20

chronic progressive disease of the brain that results in dementia. Characterized by memory loss, judgment, and visuospatial perception loss, as well as personality change

Front 21

Parkinson's

Back 21

A debilitating disease affecting motor ability
• Etiology: characterized by tremor, rigidity, akinesia and postural instability.

Front 22

Alzheimer’s:

Back 22

Development of neurofibrillary tangles and plaques that destroy cerebral tissue, altering mental functioning. Particularly noted in the hippocampus. Accompanying increased vascular degeneration is also noted in
clients with AD

Front 23

Parkinson's

Back 23

Widespread degeneration of the
substansia nigra leads to decreased levels of
Dopamine, a neurotransmitter that governs fine
motor movement along with acetycholine (ACh).
As the level of Dopamine continues to decline
more control is lost. New research that loss of
another neurotransmitter, norepinepherine,
results in progressive hypotension as well.

Front 24

Huntington’s Disease:

Back 24

A decrease in gammaaminobutyric
acid (GABA) and ACh, both
excitatory neurotransmitters, results in an
imbalance with Dopamine. The outcome is jerky,
purposeless movements of the hands, face,
tongue and legs. Progress is in 3 stages
– Stage 1-neurologic or psychological Sx
– Stage 2-Increasing dependence
– Loss of independence

Front 25

Alzheimer’s:

Back 25

Formation of beta amyloid plagues
in the precentral gyrus of the frontal brain
appears to destroy normal brain function,
interfering with reasoning nand memory
capacity. Neurofibrillary tangles cover the
neurons, interrupting signal transmission across
neuronal synapses. Vascular degeneration
occurs more rapidly than with normal aging,
increasing cerebral atrophy.

Front 26

• Parkinson’s:

Back 26

• Stoop posture, flexed trunk, wrist slightly dorsiflexed
• Gait-Slow, shuffling, short, unsure steps, difficulty
stopping quickly
• Motor-bradykinesia, akinesia, pill rolling movement,
masklike facies
• Speech-Soft, low-pitch voice, dysarthria, echolalia and
repetition of sentences

Front 27

Huntington’s:

Back 27

• Facial jerking side to side or side to center
• Rapid, purposeless tongue movement
• Lower arm and hand jerking movements
• Uncontrolled knee, leg and/or foot jerking
• Hesitant or explosive speech
• Poor balance
• Bowel and/or bladder incontinence

Front 28

• Alzheimer’s:
• Early Stage:

Back 28

• Forgets names, misplaces items
• Mild memory loss
• Short attention span
• Subtle personality changes
• Cognitive impairment, judgment
• Decreased knowledge of current events
• Wandering

Front 29

• Alzheimer’s
• Middle stage:

Back 29

• Severe cognitive impairment
• Disorientation to time, place event
• Possible depression
• Physical Impairment
• Loss of ability to care for self
• Speech and language deficits
• Incontinent
• Wandering

Front 30

• Alzheimer’s
• Late stage:

Back 30

• Completely incapacitated
• Total dependence
• Motor and verbal skills lost
• General and focal neurological deficits

Front 31

• Potential complications
• Parkinson’s:

Back 31

• Major problems with falls as disease progresses.
• Potential for aspiration as motor control deteriorates and
swallowing is less controlled

Front 32

• Potential complications
• Alzheimer’s:

Back 32

• Risk for injury due to wandering into traffic
• Potential for falls
• Potential for dehydration and malnutrition
• Possible injury to self and others
• Skin breakdown secondary to incontinence of
bowel and bladder

Front 33

• Nutritional needs
• All: Alzheimer's, Parkinson's, Hunnington's

Back 33

As each advances there is a growing risk for
aspiration, dehydration and malnutrition.
• Softer, smoother textured foods, such as pureed
foods or puddings, may be more easily
swallowed with the deterioration of muscle
control. Thickened liquids are safer than thin
liquids such as water when swallowing is hard to
control. It is important to provide calorie dense
foods as the volume consumed may decrease
over time.

Front 34

• Parkinson’s

Back 34

• Age of onset is typically between 40-70 with the
peak in the 60’s

Front 35

Hunningtons

Back 35

• Usual age of onset of symptoms is 35-50.

Front 36

• Alzheimer’s:

Back 36

• Usual onset is older than 40, and highest
incidence is after 65.

Front 37

• Hormone Production:

Back 37

• Assist in BP control by converting angiotensin I to
angiotensin II

Front 38

• Prostaglandins:

Back 38

• PGE2 and prostacyclin which help regulate glomerular
filtration, renal vascular resistance and renin production

Front 39

• Bradykinin:

Back 39

• Dilates afferent arteriole and increases capillary
membrane permeability

Front 40

• Erythropoietin:

Back 40

• Triggers RBC production in presence of decreased
oxygenation

Front 41

• Clinical Manifestations of Altered Renal
Function
• Lab:

Back 41

• Elevated creatinine level (specific to renal
function)
• Decreased 24 hour creatinine clearance
(normal is 90-139 ml/min for male and 80-
125 ml/min for women)
• Electrolyte imbalances

Front 42

• Creatinine:

Back 42

End product of muscle and protein
metabolism. Is a direct measure of renal function
because muscle mass and metabolism is fairly
constant
• Men- 0.6-1.2 mg/dl
• Females- 0.5/1.1 mg/dl

Front 43

BUN:

Back 43

• Measure level of urea nitrogen and is an indirect
measure of renal elimination of urea. Nor
specific to renal function

Front 44

• Stress Incontinence:

Back 44

• Loss of urine during coughing, sneezing,
jogging or lifting. Results from weakening
of the bladder neck supports and/or
urethral sphincter weakness

Front 45

Urge incontinence:

Back 45

• Involuntary loss of urine associated with a
sudden urge to void. Clients cannot
suppress the signal relaxing the urethral
sphincter

Front 46

• Reflex incontinence:

Back 46

• Abnormal flexion of the detrusor muscles
causing bladder contraction and voiding
• Associated with central nervous system
lesions from stroke or spinal lesions from
traumatic injury or CA

Front 47

• Overflow incontinence

Back 47

• Involuntary loss of urine due to over
distension of the bladder. Often associated
with a neurological problem causing a lack
of the sensation that notifies the client of
need to void. May also be associated with
enlarge prostate, genital prolapse (in
women)

Front 48

• Functional incontinence:

Back 48

• Leakage of urine caused by factors other
than a disease of the lower urinary tract
• Common cause is dementia, where the
client is unable to interpret the need to
urinate with a need to go to a bathroom
facility (not go in public)

Front 49

• Cystitis:

Back 49

• An inflammation of the bladder. Most commonly
caused by in infectious agent, 90% of which are
E. Coli. The organisms first grow in the perineal
area and then invade the urinary bladder. Most
common cause of infection is poor hygiene.
• Patho: Bacteria move up the urethra and into the
bladder, resulting in an inflammatory response,
elevation of white (See table 73-2, p. 1679)

Front 50

Urethritis:

Back 50

• Inflammation of the urethra that results in
symptoms similar to the inflammatory symptoms
of UTI. Common causes in men are STDs
(gonorrhea) and non-specific urethritis.
• In women the causes may be an STD or the
same cause as cystitis
• Patho: Bacteria enter the urethra and trigger
inflammatory response, often resulting in whitish
exudate from the meatus

Front 51

• Pyelonephritis:

Back 51

• Infection or the effects of infection in the
kidney.
• Acute pyelonephritis may result from an
acute UTI with bacteria traveling up the
ureters and into the kidney. Chronic
pyelonephritis is the result of chronic or
repeated infections of the kidney

Front 52

• Cystitis:

Back 52

• Frequency, urgency, and dysuria
• Potentially:
– Cloudy urine
– Foul smelling urine
– Blood in urine
– Abdominal cramping

Front 53

• Urethritis

Back 53

• Burning on urination
• Discharge from the penis, urethral meatus
or vagina and/or lower abdominal
discomfort.

Front 54

• Pyelonephritis:

Back 54

• Flank pain, abdominal pain, low grade
fever

Front 55

• Possible complications
• Cystitis:

Back 55

• Scarring of the urinary bladder,
septicemia, urethral stricture from scarring,
pyelonephritis

Front 56

• Possible complications
• Urethritis:

Back 56

• urethral stricture from scarring, cystitis,
pyelonephritis

Front 57

• Possible complications
• Pyelonephritis:
•

Back 57

Septicemia
• Septic shock
• Renal failure
• Scarring of the renal system

Front 58

Retinopathy:
complication of diabetes

Back 58

Related to blockage of retinal
blood vessels and leakage, leading to
retinal hypoxia. Occurs in almost 100% of
type I by 20 years of disease progression
and 78% of type II. Associated with fasting
blood glucose levels >129 mg/dl.
Accompanying hypertension increases the
risk.

Front 59

Neuropathy:
Diabetic complication

Back 59

May be focal or
diffuse, and the most common are diffuse
in nature. Hyperglycemia leads to
neuropathy through blood vessel changes
that lead to nerve tissue hypoxia and
damage to both the axon and the myelin
sheath. Excess glucose is converted to
sorbitol which coats the nerve sheath
interrupting nerve conduction.

Front 60

• Male Erectile Dysfunction:
Diabetic complication

Back 60

Occurs at a
higher rate and earlier in men with DM.
Associated with a combination of
neuropathy, vascular occlusions and other
problems. Psychological factors can play a
large part and cannot be overlooked.

Front 61

Leg and Foot complications:
Diabetic complication

Back 61

• Primarily result from the vascular occlusive side
effects and neuropathies associated with DM.
Build up of plagues in the arterial circulation
decreases cellular perfusion leading the tissue
hypoxia and slow healing of wounds. This also
increases risk for infection due to decreased
availability of WBC’s and supportive proteins.

Front 62

• Integumentary problems
Diabetic complication

Back 62

are associate with
tissue hypoxia due to vascular occlusion. The
resultant tissue weakness makes the system
more susceptible to injury and delayed healing

Front 63

• Infections:
Diabetic complication

Back 63

As already noted tissue hypoxia
results in skin susceptibility to injury with delayed
healing, lack of immune bodies to fight infection
and decreased availability of nutrients to build
new tissue

Front 64

Type I DM

Back 64

only treatable by insulin
because there is no insulin production

Front 65

– Sulfonylureas

Back 65

-Stimulate insulin production

Front 66

– Meglitinides

Back 66

-Stimulate insulin production

Front 67

– Biguanides-

Back 67

Decreases liver glucose release
and decreases cell resistance to insulin

Front 68

Alpha-Glucsidase inhibitors:

Back 68

slow intestinal
digestion and absorption of CHO, reducing
rate of glucose absorption

Front 69

• Thiazolidinedione agents:

Back 69

enhance insulin
action, promoting glucose use in
peripheral tissues