Patho Quiz 2 Flashcards

1
Q

What clinical manifestations will occur in panhypopituitarism?

A
Abnormal slowing of growth
Delayed puberty
Excessive thirst and excessive urination
Less frequent menstrual periods
Low blood sugar (hypoglycemia)
Prolonged jaundice in infants
Sensitivity to cold
Poor appetite
Weight loss or weight gain
Unusually dry skin
Nausea or dizziness Fatigue or drowsiness
Small penis in males
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2
Q

What clinical manifestations occur with excess growth hormone?

A

Growth hormone (GH) is secreted by the anterior pituitary and regulates metabolic processes related to growth. An excess in GH can occur due to a tumor of the anterior pituitary gland. Interestingly, there are different manifestations of excess GH depending on the age/growth status of the affected individual.

Children/Adolescents - in those whose bones have not stopped growing yet, an increase in GH causes gigantism.
Skeletal growth is excessive, and some children may reach heights of 8-9 feet tall.
Adults - the skeletal bones have stopped growing, so an increase in GH, termed acromegaly, causes bony and connective tissue growth in certain areas (see below).
Frontal bossing - protrusion of the forehead
Macrognathia - protruding jaw
Large hands and feet
Macroglossia - enlarged tongue
Hyperglycemia - GH inhibits uptake of glucose by cells and increases the liver’s production of glucose –> high glucose levels
Diabetes mellitus eventually occurs

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3
Q

What clinical manifestations occur with SIADH?

A

Kidneys retain water causing diluted blood (Serum hypoosmolality). Sodium is then diluted in the blood causing (Hyponatremia). Severe Hyponatremia can lead to confusion, lethargy and seizures.

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4
Q

What causes diabetes insipidus?

A

Insufficient activity of ADH results in diabetes insipidus. It can be caused by too little secretion of ADH from the posterior pituitary or inadequate response of the kidney to normal amounts of ADH

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5
Q

What clinical manifestations occur with diabetes insipidus?

A

Patient can develop severe dehydration if they’re not able to continuously drink fluids and can experience excessive thirst (Polydipsia). Excessive amounts of urine (Polyuria) can be as much as 8-12 liters per day. Hypoosmolality (dilute urine) develops in patients with diabetes insipidus.

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6
Q

What does negative feedback mean in relation to thyroid hormone?

A

The thyroid gland is influenced by both the hypothalamus and the anterior pituitary, collectively called the hypothalamic-pituitary axis (HPA). The hypothalamus, when stimulated, secretes thyrotropin-releasing hormone (TRH) which in turn stimulates the anterior pituitary to release thyroid-stimulating hormone (TSH). TSH in turn stimulates the thyroid gland itself to release thyroid hormones, T3 and T4. Thyroid hormone levels in the bloodstream have a direct effect on both the hypothalamus and the anterior pituitary.

A negative feedback system is in place to prevent overstimulation of the HPA and over-secretion of the above hormones. A negative feedback system can be thought of as a system of checks and balances between the the HPA and the thyroid gland so that (ideally) as thyroid hormone levels rise, the HPA will be inhibited so that TRH and TSH will not be released.

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7
Q

What clinical manifestations occur with hypothyroidism and hyperthyroidism?

A

Hypothyroidism: hypotension, bradycardia, weight gain, constipation, and cold intolerance (slight decrease in body temperature).

Severe/long-standing hypothyroidism: causes puffiness around eyes, hands, and feet. Manifestations of infants borns with hypothyroidism: excessive sleeping, bradycardia, cold mottled skin, weak hoarse cry, and difficulty eating due to protruding tongue.
Hyperthyroidism: hypertension, tachycardia, weight loss, diarrhea, and heat intolerance (slight increase in body temperature).

Graves disease: underlying cause of 50-80% of cases of hyperthyroidism. Manifestations include exophthalmos, or protrusion of the eyeball. Fat accumulation, inflammation, and edema of the orbital cause exophthalmos. If untreated, graves disease can lead to a life threatening complication called thyrotoxic crisis of thyroid storm.

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8
Q

What are causes of hypothyroidism?

A

Hypothyroidism is the deficient production of thyroid hormone and is the most common disorder of thyroid function. In hypothyroidism, the decrease in thyroid hormone leads to excessive TSH secretion by the anterior pituitary (due to the negative feedback system - the anterior pituitary is trying to get the thyroid gland to ramp up production of thyroid hormone). The most common causes are hypothyroidism are:

Autoimmune (Hashimoto’s disease) - the patient’s immune cells attack the thyroid cells
Post-surgical or radioactive treatment for hyperthyroidism - with the thyroid removed or ablated, it is unable to produce thyroid hormone
Post-radiation treatment of head/neck cancer
Iodine deficiency - the thyroid uses iodine to produce thyroid hormone

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9
Q

What causes a goiter?

A

Both hyperthyroidism and hypothyroidism can cause a goiter (or the enlargement of the thyroid gland).

In hyperthyroidism, continual stimulation of TSH receptors on the thyroid gland, like Graves disease, will cause a goiter.

In hypothyroidism, a decrease in the thyroid hormone leads to excessive TSH secretion and continual stimulation of the thyroid gland will cause a goiter.

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10
Q

What clinical manifestations occur with hypo and hyperparathyroidism?

A

Hypoparathyroidism:

Causes hypocalcemia and hyperphosphatemia
Hypocalcemia symptoms include tetany (or muscle spasms), cardiac dysrythmias, and burning/tingling of the hands, feet, lips, and tongue

Hyperparathyroidism:

Causes hypercalcemia and hypophosphatemia
Hypercalcemia symptoms include confusion, anorexia, abdominal pain, muscle pain, weakness, and pathologic bone fractures. Kidney stones leading to renal infections can occur due to the increased calcium being filtered through the kidney.

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11
Q

Which substance is controlled by parathyroid hormone?

A

When blood calcium levels decrease, parathyroid hormone is released. Parathyroid hormone causes bones to release calcium, the kidneys to reabsorb more calcium, and the intestines to absorb more calcium. As a result, blood calcium levels increase. Once they reach a certain level, calcitonin is released to decrease the level. Calcitonin and PTH work together to maintain calcium levels.

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12
Q

What clinical manifestations occur in pheochromocytoma?

A

Clinical manifestations: hypertension, tachycardia, palpitations, and headache due to the effects of catecholamines of the cardiovascular system. Cardiac dysrhythmias and heart failure may result. Sweating, hyperglycemia, constipation, and weight loss may also occur.

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13
Q

Differentiate Cushing Disease from Addison Disease.

A

Cushing’s disease and Addison disease are basically the exact opposite.
Cushing disease is an increased secretion of cortisol while Addison’s is an underproduction of cortisol in the body.

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14
Q

What clinical manifestations occur with Cushing Disease?

A

Fat in the face (Moon Face), Buffalo hump, Central obesity, Purple Striae (Stretch marks), Weight gain, Elevated blood pressure.

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15
Q

What clinical manifestations occur with Addison Disease?

A
  • Addison Disease is caused by inadequate glucocorticoid and mineralcorticoid secretion.
  • Weakness and fatigue are the early symptoms.
  • Lack of cortisol causes hypoglycemia and an inability to handle stress.
  • Lack of aldosterone causes sodium and water loss resulting in hypotension and dehydration.
  • Potassium retention causes hyperkalemia.
  • Addisonian crisis where hypotension progresses to complete vascular collapse and shock.
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16
Q

What clinical manifestations occur in diabetes mellitus due to microvascular complications?

A

Damage is due to chronic hyperglycemia. This damage leads to complications such as retinopathy and possible blindness, nephropathy and possible renal failure, and neuropathy (damage to nerves) that causes sensory changes in hands and feet leading to sensations of numbness, pins and needles and pain

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17
Q

What five criteria are used to establish the diagnosis of metabolic syndrome?

A
  1. increased waist circumference (over 40’’ in men and over 35’’ in women)
  2. plasma triglycerides at or above 150mg/dL
  3. plasma high-density lipoproteins (HDL; which is good cholesterol); less than 40mg/dL in men and less than 50mg/dL in women
  4. blood pressure at or above 130/85
  5. fasting plasma glucose at or above 110mg/dL
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18
Q

What clinical manifestations occur with diabetic ketoacidosis?

A

DKA is an acute complication of diabetes mellitus, most often found in Type 1 Diabetes. Lack of insulin leads to the catabolism of lipids for ATP. This process produces byproducts called ketones, which are acidic due to their chemical composition.

Clinical Manifestations of Diabetic Ketoacidosis (DKA):

Labs:

Blood pH decreases <7.35
Blood glucose levels increase
Blood glucose ~>250 mg/dL causes polyuria and hypovolemia.
Electrolyte losses via polyuria can cause hypokalemia.
Assessment:

Patient’s breath has a distinct “fruity” smell- due to ketones.
Respirations are deep and rapid- due to lungs compensation for metabolic acidosis

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19
Q

Which part of the nervous system controls internal organs such as the heart and intestines?

A

The contraction of both smooth muscle and cardiac muscle is controlled by motor neurons of the autonomic nervous system

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20
Q

Differentiate the responses when the sympathetic and parasympathetic nervous systems are stimulated.

A

When the sympathetic nervous system is stimulated, it causes pupillary dilation, increase in heart rate and force of contraction, bronchodilation, glycogen breakdown to glucose b the liver, secretion of epinephrine and norepinephrine from the adrenal medulla. Flow of saliva, intestinal peristalsis and secretion and bladder contraction are inhibited.

When the parasympathetic nervous system is stimulated, the sympathetic nervous system are relaxed or inhibited. The pupil constricts, heart rate decreases and bronchi constrict. Functions used during eating and drinking are stimulated. Rate of saliva and intestinal peristalsis and secretion increase. The liver releases bile to digest fat and the bladder contracts.

21
Q

Which nerve is most likely to regenerate?

A

The nerves that are most likely to regenerate are PNS nerves- due to the nature of the myelin sheaths created by Schwann’s cells.
This is in comparison to Oligodendrocytes within the CNS producing myelin sheaths, which are more prone to inflammation.
Other factors in nerve regeneration include the nature of an injury.
“Crush” injuries are more likely to regenerate as opposed to “cut” injuries.
Cut injuries lead to the formation of connective tissue scarring.

22
Q

Which neurotransmitters are associated with amyotrophic lateral sclerosis?

A

The neurotransmitters associated with ALS (aka Lou Gehrig’s disease) are glutamate and aspartate. Which are excitatory neurotransmitters that increase sensitivity to painful stimuli.

23
Q

Differentiate where the bleeding occurs in epidural, subdural, and subarachnoid hematomas.

A

Epidural hematomas: outside the dura mater or between the dura mater and the skull

Subdural hematomas: from subdural veins collects blood between the dura mater and the arachnoid

Subarachnoid hematomas: between the arachnoid and the pia mater (rupture of an aneurysm or bleeding from AVM) at the base of the brain

24
Q

What clinical manifestations occur with an epidural hematoma?

A
  • loss of consciousness, followed by alertness, then loss of consciousness again
  • severe headache, nausea, vomiting, dizziness, confusion
  • ipsilateral pupil dilation (enlarged pupil on side of hematoma)
  • contralateral hemiparesis (weakness of body opposite hematoma)
25
Q

What clinical manifestations occur with bacterial meningitis?

A

infectious signs: fever, tachycardia, chills, petechial rash

meningeal signs: severe throbbing headache, severe photophobia, nuchal rigidity (stiff neck), positive Kernig (pain in the back of the neck when the knee is straightened from a flexed hip and knee position), and Brudzinski (neck pain and flexion of the knees and hips with passive flexion of the neck) signs

neurologic signs: decrease in consciousness, hemiparesis/hemiplegia, projectile vomiting

26
Q

What provides an alternative route for blood flow in the brain when one of the major arteries is obstructed?

A

The Circles of Willis

27
Q

Which cranial nerves control eye movement?

A

Cranial nerves III, IV and VI, which are located in the brain stem

28
Q

Which cranial nerve controls pupillary size?

A

Oculomotor (III)

29
Q

Which cranial nerves control taste and movement to the tongue?

A

The olfactory, facial, glossopharyngeal, and vagus nerves control taste and movement of the tongue.

Olfactory - carries impulses for sense of smell, which is important for taste

Facial - sensory nerve for anterior 2/3 of tongue

Glossopharyngeal & Vagus - sensory and motor impulses for the tongue and throat, taste for posterior 1/3 of tongue

30
Q

Which cranial nerve controls balance?

A

Vestibulocochlear (VIII)

31
Q

What clinical manifestations occur when cranial nerve #12 hypoglossal is damaged?

A

Hypoglossal cranial nerve 12 is the motor for the tongue. To check for dysfunction you can ask the patient to open their mouth but keep his tongue inside. Also, ask the patient to stick tongue straight out. If the hypoglossal nerve is damaged there will be fasciculations (twitching) when the tongue is in the mouth or deviation to one side when the tongue is sticking out.

32
Q

What dermatome levels supply the nipple line, tip of sternum, and umbilicus?

A

T4 the nipple line

T6 the tip of the sternum or the xiphoid process

T10 the umbilicus

Dermatone levels can be used when describing the area of involvement after spinal cord injuries and to describe the level of anesthesia after a spinal anesthetic.

33
Q

Which part of the nervous system carries pain signals from the internal organs?

A

autonomic nervous system

34
Q

What are Cheyne-Stokes respirations?

A

Cheyne-Stokes respirations are an abnormals pattern of breathing with alternating periods of tachypnea (respiratory rate greater than 20 breaths per minute in adults) and apnea (no respiration). The respirations increase in rate and depth followed by a decrease in rate and depth followed by a decrease in rate and depth with an eventual pause in respirations.

35
Q

What pupillary response is expected if the patient has severe ischemia and hypoxia to the brain?

A

Severe ischemia and hypoxia to the brain or compression of the brain stem usually produces fixed dilated pupils. Pupillary changes corresponds to the level of consciousness and indicate the presence of brain stem dysfunction because the area that controls the arousal is adjacent to the area that controls the pupils in the brain stem.

36
Q

What does an abnormal and absent oculovestibular reflex indicate?

A

The oculovestibular reflex is tested by injecting ice water into the outer ear of a patient with a decreased level of consciousness. The tympanic membrane must be determined to be intact so the water doesn’t inject into the middle ear. An abnormal oculovestibular reflex occurs when the eyes do not move together (dysconjugate) indicating some injury to the brain stem. Absent response is no eye movement with the eyes staying midline and indicates severe injury to the brain stem

37
Q

Differentiate decorticate and decerebrate posturing in relation to patient positioning and damage to brain structures.

A

Decorticate posturing is flexion of the arms, wrists, and fingers with extension, internal rotation, and plantar flexion of the lower extremities. Decorticate posturing occurs when there is an injury to the cerebral hemispheres but not the brain stem.
Decerebrate posturing is all four extremities in rigid extension with hyperpronation of the forearms and plantar flexion of the feet. This indicates injury to the cerebral hemispheres and the brain stem.

38
Q

What is normal intracranial pressure?

A

Intracranial pressure is normally 1-15 mm Hg or 60-180cm H2O

39
Q

What is cerebral autoregulation?

A

Cerebral autoregulation is the process to maintain homeostasis in the brain. Normally, when hypoxia, hypercapnia or acidosis, they cerebral vessels dilate to increase oxygen levels, decrease CO2 levels and increase the pH. During stage three of increase intracranial pressure, this process is lost.

40
Q

What clinical manifestations occur in each stage of increased intracranial pressure?

A

Stage 1:

  • cerebral blood vessels constrict and cerebrospinal fluid is forced out of cranial vault, patient is awake and alert, pupils are equal and react quickly to light, vitals are normal

Stage 2:

  • arterioles throughout body constrict, patient becomes confused, restless, drowsy, pupils are still equal and of normal size, pupils react slower than normal to light, slight slowing of respiratory rate

Stage 3:

  • patient is unable to stay awake, pupils are equal and normal size but react sluggishly, systolic pressure increases and diastolic pressure decreases, heart rate slows

Stage 4:

  • patient progresses into a coma, ipsilateral dilation and fixation of pupil occur, pupil on side of hemorrhage becomes fixed and dilated, hyperventilation occurs, patient will pass away
41
Q

Which pupil will fix and dilate if there is severe damage on the right side of the brain?

A

The pupil on the side of the problem becomes fixed and dilated first, but eventually both pupils become fixed and dilated.

42
Q

Differentiate brain death and cerebral death.

A

Cerebral death is an irreversible state where the death of the cerebral hemispheres has occurred but not the brain stem or cerebellum the patient will not be able to respond to the environment or speak.

The patient will show symptoms such as:

  • heart rate and breathing maintained without support
  • bowel and bladder incontinence
  • If the patient is in a coma there will be no wakefulness or awareness, no eye-opening
  • If the patient is in a vegetative state there will be partial wakefulness, not true awareness, eyes open spontaneously. The longer they are in a vegetative state the less likely the patient will regain awareness.

Brain death is an irreversible cessation of brain function including the cerebral hemispheres, the brain stem, and the cerebellum. The brain is severely damaged and will not be able to maintain homeostasis. Six requirements are done to declare a patient brain dead such as:

  1. All procedures and therapeutic procedures must be completed to declare no possible function of the cerebral hemispheres, brain stem, and cerebellum
  2. patient is in an unresponsive coma with no motor or reflex movements
  3. unable to maintains body’s internal homeostasis
  4. no spontaneous respirations
  5. no oculomotor responses; dilated fixed pupils
  6. flat EEG for 6-12 hours
43
Q

Which type of seizure does not cause a loss of consciousness?

A

The types of seizures that do not cause a loss of consciousness are Partial Simple.

44
Q

What function does a patient have with a C5 spinal cord injury that helps prevent pressure ulcers?

A

patients with C5 injury will have control of the head, neck, and shoulders. Shoulder control allows the patient to lean forward or side-to-side to relieve pressure on the skin and prevent pressure ulcers.

45
Q

Which life-threatening complications can occur with a cervical spinal cord injury?

A

cord swelling can be life-threatening because it may impair the diaphragm by compressing the phrenic nerve as it exits the spinal canal at C3 to C5. The phrenic nerve innervates the diaphragm. Swelling in the cervical area can also compromise functions mediated by the medulla oblongata (brain stem) such as respiratory and cardiac functions.

46
Q

What clinical manifestations occur with autonomic hyperreflexia? With spinal shock?

A

Autonomic Hyperreflexia clinical manifestations are: an injury to T6 and above, causes severe hypertension (300 systolic), severe bradycardia (30-40 bpm), flushed skin above lesion, and pallor below lesion. Spinal shock has reflex function completely lost below injury- all skeletal muscles- bladder, bowel, sexual function- and autonomic control. Occurs immediately after injury and can last days to months.

47
Q

What causes autonomic hyperreflexia?

A

occurs in patients with spinal cord injuries at the T6 or above level and is due to overactivity of the autonomic nervous system.

48
Q

What clinical manifestations occur with Alzheimer Disease?

A

Clinical manifestations occur with Alzheimer Disease: memory loss, mood changes, and behavioral changes.