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Advanced Pathophysiology > Endocrine/Neuro > Flashcards

Endocrine/Neuro Flashcards

1
Q

this system regulates growth maturation, metabolic function, fluid balance, responses to stress, and reproduction through the action of the hormones they secrete

A

endocrine system

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2
Q

endocrine disorder that is an intrinsic malfunction of the hormone-producing gland

A

primary

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3
Q

endocrine disorder that results from an abnormal pituitary secretion of trophic hormones signals (main problem)

A

secondary

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4
Q

feedback loop Figure 20-2B!!!!

A

Study It!!

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5
Q

type of thyroid disorder in which the thyroid glad itself fails:
o inadequate hormone produced by the thyroid
–> low levels of circulating hormone
o blood levels of the corresponding trophic pituitary hormone are very elevated

A

Primary

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6
Q

type of thyroid disorder in which the pituitary gland fails:
o release of the trophic hormone is significantly decreased –> Secondarily reducing primary gland function so both levels are abnormally low thyroid hormones

A

Secondary

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7
Q

T3 and T4 are regulated by the ______ ______ ______ that is secreted from the anterior pituitary

A

thyroid stimulating hormone (TSH)

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8
Q

thyroid stimulating hormone (TSH) is secreted from the _________

A

anterior pituitary

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9
Q

Thyroid hormones produced in the follicular cells of the thyroid that regulate metabolism, required for growth and development of tissue

A

o T3 – triiodothyronine

o T4 – thyroxine

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10
Q

“Thyrotoxicosis”– condition that results from any cause of increased TH levels

A

hyperthyroidism

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11
Q

Types of _________:
o Hashimotos- first stages of Hashimotos when there is a release of T3 and T4 d/t thyroid cell destruction (hyperthyroidism)
o Toxic multi nodular goiter
o Solitary toxic adenoma

A

Hyperthyroidism

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12
Q

the most common cause of hyperthyroidism that is a result of stimulation of thyroid cells with autoantibodies against TSH receptor (Type II hypersensitivity where the target cells of the thyroid are not destroyed but malfunction)

A

Grave’s Disease

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13
Q

Patho of _______:
 Auto-antibodies bind and activate with receptors for TSH and stimulate production of T4
 As the T4 rises in the system, the pituitary decreases the production of TSH
 The etiology is autoimmune (Grave’s Disease genetic markers)
 Feedback loop out of commission

A

Grave’s Disease

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14
Q 
Clinical Manifestations of \_\_\_\_\_\_\_:
>Adrenergic stimulation – d/t increase in T4
tachycardia
nervousness
lid lag (associated w/ exophthalmos)
tremor
increased B/P
>Excess T4 
increased O2 consumption
changes in protein metabolism
increase in metabolic rate
decrease in weight
heat intolerance
inability to concentrate
amenorrhea in women (scant menses)
>Immunologic stimulation – goiter
A

Grave’s Disease

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15
Q

Triad of Symptoms of Grave’s Disease

A

o Hyperthyroidism
o Exophthalmos
o Goiter

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16
Q

very high levels of T4 that is life-threatening resulting in increased temperature, severe tachycardia, arrhythmias, congestive heart failure, extreme restlessness, psychosis
***may be triggered via stress or gland manipulation in people who have hyperthyroidism

A

Thyroid Storm

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17
Q

type of hypothyroidism that accounts for the majority of cases d/t the intrinsic thyroid gland dysfunction that results from:
o Congenital, defective hormone synthesis, iodine deficiency, anti-thyroid drugs, iatrogenic loss of thyroid tissue
o Congenital aka critinism d/t thyroid dysgenesis or lack of development of thyroid gland

A

Primary

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18
Q

type of hypothyroidism that is related to pituitary or hypothalamic failure (usually r/t head or brain conditions) caused by pituitary tumor or treatment of tumor

A

Secondary

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19
Q

Labs for Diagnosis of ______:
o Low T4 (b/c thyroid is not producing it the way it should)
o High TSH (b/c the anterior pituitary is trying to get the thyroid to produce more T4)

A

Hypothyroidism

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20
Q

Causes of _______:
o Acute and subacute thyroiditis
o painless thyroiditis
o postpartum thyroiditis

A

Primary Hypothyroidism

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21
Q

with a patho similar to Hashimoto, this generally occurs 6-12 months postpartum with spontaneous recovery in most cases

A

postpartum thyroiditis

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22
Q

Most common cause of acquired hypothyroidism caused by gradual inflammatory destruction of thyroid tissue by circulating auto-antibodies and infiltration by lymphocytes

A

Hashimoto’s (Lymphocytic Thyroiditis or Autoimmune Thyroiditis)

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23
Q

Diagnosis of ______:

presence of thyroperoxidase and thyroglobulin antibodies

A

Hashimoto’s

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24
Q

lack of iodine results in lack of ___ and ___

A

T3 and T4

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25
Q

lack of T3 and T4 stimulates TSH secretion which causes the thyroid cells to secrete large amounts of thyroid globulin which leads to ______

A

goiter

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26
Q

type of hypothyroidism caused by radiation of the thyroid gland or when they surgically remove the thyroid gland

A

iatrogenic

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27
Q

Lab Diagnosis of ______:
Decreased T3 & T4 which leads to…
Increased TSH
**Sensitive test we have for TSH is going to start detecting elevation levels of TSH before we have a significant amount of drop in the T3 and T4 & is used as a screening device and a monitoring device.

A

Hypothyroidism

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28
Q 
Clinical Manifestations of \_\_\_\_\_\_\_ in \_\_\_\_\_\_:
dull appearance
thick-protruding tongue
thick lips
prolonged jaundice
poor muscle tone
umbilical hernias are common
bradycardia with a hoarse cry
mental retardation if not treated
A

Hypothyroidism in Newborns

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29
Q 
Clinical Manifestations of \_\_\_\_\_\_\_ in \_\_\_\_\_\_\_ and \_\_\_\_\_\_:
decrease metabolic rate
weakness
lethargy
cold intolerance
decrease appetite
bradycardia
moderate weight gain
elevated serum cholesterol and triglycerides
enlarged thyroid
dry skin
constipation
depression
loss of lateral portion of eyebrow
women- irregular menses
A

Hypothyroidism in Children and Adults

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30
Q

generalized non-pitting edema, decreased level of consciousness, hypotension, hypothermia that occurs in severe or prolonged hypothyroidism and may progress into coma

A

myxedema

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31
Q

system that provides precise monitoring and control of the cellular environment which is important for maintaining hormone levels within physiologic ranges

A

feedback systems

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32
Q

Most common type of feedback that occurs when a changing chemical, neural, or endocrine response decreases the subsequent synthesis & secretion of a hormone
 Regulation is possible at 3 levels

A

Negative Feedback

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33
Q

Possible Regulation Levels of _______:
• Target organ (ultra-short feedback)
• Anterior pituitary (short feedback)
• Hypothalamus (long feedback)

A

Negative Feedback

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34
Q

Type of feedback that occurs when a chemical, neural, or endocrine response increases the synthesis and secretion of a hormone or when an increased hormone level further increases the synthesis and secretion of that same hormone

A

Positive Feedback

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35
Q

TH is regulated through a ______ feedback loop

A

negative

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36
Q

TH negative feedback loop involves the ______ (3)

A

hypothalamus
anterior pituitary
thyroid gland

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37
Q

TH negative feedback loop is initiated by _______

A

TRH (thyrotropin-releasing hormone)

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38
Q

________ is synthesized and stored in the hypothalamus

A

TRH (thyrotropin-releasing hormone)

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39
Q

TRH (thyrotropin-releasing hormone) levels increase with exposure to ______ or ______ and from decreased levels of _____

A

cold or stress/ T4

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40
Q 
Regulation of \_\_\_\_\_\_\_\_\_\_:
TRH is released into the hypothalamic-pituitary portal system 
-->Circulates to the anterior pituitary
-->stimulates release of TSH
-->causes release of stored TH
-->increase in TH synthesis
A

Thyroid Hormone Secretion

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41
Q

As levels of TH rise, there is a negative feedback effect on the HPA that inhibits release of _____ and ____
–>results in decreased TH synthesis and secretion

A

TRH and TSH

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42
Q

DM caused by absolute insulin deficiency caused by the destruction of the beta cells of the Islet of Langerhans of the pancreas

A

DM Type I

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43
Q

DM caused by insulin resistance in peripheral tissue so there is a deficient amount of insulin secreted from the pancreas

A

DM Type II

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44
Q

insulin helps glucose enter into the _____(3)

A

liver (glycogen)
muscles (energy)
adipose tissue (fat)

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45
Q

Glucose is supplied to the blood stream from the ____ and _____

A

GI track and the liver

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46
Q

Glucose is more abundant in ______ than in _____

A

extracellular fluid than inside cells

47
Q

major glucose transporter for the blood brain barrier that is insulin independent (they can be transported across the cell membrane for a specific tissue without insulin)

A

Glut 1

48
Q

glucose transporter in the liver and in a small part in the pancreatic beta cells that is insulin independent (they can be transported across the cell membrane for a specific tissue without insulin)

A

Glut 2

49
Q

glucose transporter needed for glucose to be used by the neurons that is insulin independent

A

Glut 3

50
Q

the only Insulin DEPENDENT glucose transporter found in muscle and adipose tissue

A

Glut 4

51
Q

If there is no insuline, Glut 4 is sequestered in the _______

A

vesicles of the cells

52
Q

In the presence of insulin, Glut 4 will move to the ______ to allow glucose to enter into the cell

A

plasma membrane

53
Q

Type I DM affects more _____

A

males

54
Q

Type I DM risk marker chromosome

A

human leukocyte antigen gene on chromosome 6

55
Q

Congenital Nature of _____:
virus or other environmental insult occurs
–>insulin auto-antibodies and glutamic acid decarboxylase are produced
–>damage to the islet cells
–>Hyperglycemia

A

DM Type I

56
Q

total absence of insulin and excessive glucagon d/t an increase in glucose that does not shut down the production of glucagon in the liver

A

Hyperglycemia

57
Q

Patho of ______:
There is a genetic predisposition and environmental factors that combine to produce autoantigens that form on the insulin producing beta cells and circulate in the blood stream. This leads to a processing and presentation of autoantigen by Antigen Presenting Cells (APC’s) and the activation of the T-Helper 1 and T-Helper 2 lymphocytes
Fig 21-13

A

DM Type I

58
Q

stage of beta cell destruction in Type I DM of Macrophage Activation in which lymphocyte and macrophage infiltration of the islets results in inflammation (insulinitis) and islet beta-cell death

A

Stage A

59
Q

stage of beta cell destruction in Type I DM of Autoantigen Specific T Cytotoxic Cells Activation that consists of production of autoantibodies against islet cells, insulin, glutamic acid decarboxylase (GAD), and other cytoplasmic proteins

A

Stage B

60
Q

Activation of B-Lymphocytes to produce Islet cell autoantibodies and destruction of the beta cells then follows with corresponding decrease in insulin secretion
 Relative inactivity of T reg cells that contribute to a decrease in beta-cell mass and insulin production

A

Stage C

61
Q

At Risk Ethnicities for _____:
Native Americans (Southwestern- Pima Indians)
Hispanics
Blacks

A

DM Type II

62
Q 
Risk Factors for \_\_\_\_\_\_:
Age >40 
Obesity (most powerful risk factor)
family history
member ethnic minority
female
A

Type II DM

63
Q

Patho of _____:
o Genes influence insulin resistance (60-80% of cases of DMII) or beta cell dysfunction with the underproduction of insulin OR both
o May also see abnormal glucagon secretion (important in relation to prescribing pharm)
o Beta cell function (or dysfunction) is affected due to amyloid deposits (fatty deposits in pancreas and liver) or pancreatic fibrosis or cytokine toxicity
 insulin is still produced for a time but eventually there will be complete destruction and the insulin will be completely gone

A

DM Type II

64
Q

In ______, glucose enters the blood stream and the pancreas produces insulin, but it may not be enough to overcome the peripheral insulin resistance. This glucose is unable to enter the body cells effectively and glucose levels increase in the blood stream.

A

Type II DM

65
Q

the fetal siphon needs ___ mg/kg every minute per kg of the fetal weight for every minute during gestation

A

6

66
Q 
Risk Factors for \_\_\_\_\_:
family history (esp 1st degree relative)
ethnic group
age >25 years old
prior history of GDM or PCOS
overweight
Hx of OB complication
Hx of large baby greater 4000g
miscarriage 2-3 times
having a baby with a congenital anomaly
A

Type II DM

67
Q

Insulin deficiency and an increase in the insulin counterregulatory hormones (i.e., catecholamines, cortisol, glucagon, and growth hormone

A

Ketoacidosis

68
Q

In ketoacidosis,
Hepatic glucose production ______ and
peripheral glucose usage _______

A

increases

decreases

69
Q

In ketoacidosis, _________ decreases the pH (acidic) of the blood, creating a metabolic acidosis

A

ketogenesis (breakdown of ketones)

70
Q

compensation for metabolic acidosis in ketoacidosis is________

A

Kussmaul respirations (trying to blow of acid)

71
Q 
DM Type 2 complication that occurs more often in elderly patients (in particular---elderly pts with comorbidities) in which there is an increase in glucose, increase in serum osmotic pressures that leads to:
•	severe dehydration
•	low blood volume
•	low perfusion pressure
        death if it is not corrected
A

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome (HHNK Syndrome)

72
Q

Hypoglycemia followed by a rebound hyperglycemia that occurs d/t the counter-regulatory hormones that are stimulated by the hypoglycemia (glucagon, epinephrine/adrenaline, cortisol, and growth hormone)
**usually triggered (the up and down effect) by an excessive carbohydrate intake that starts the up-and-down

A

Somogyi Effect

73
Q

recurrent or persistent hyperglycemia that will cause glucose binding to the red blood cells (RBCs)

A

Non-enzymatic glycosylation

74
Q

what we are measuring when we measure Hgb A1C

A

Glycosylated Hemoglobin

75
Q

glycosylation that binds to collagen and other proteins in blood vessel walls in the intestinal tissue & will cause tissue injury associated with diabetes (i.e., injuries to the kidneys, blood vessels, peripheral nerves, and the eye lenses

A

Advanced Glycosylation End Products – AGEs

76
Q

Patho of _______:
 Cross-linking and trapping of proteins, albumin, LDL, immunoglobulin, and complement with thickening of the basement membrane or increased permeability in small blood vessels and nerves
 Binding to cell receptors (such as macrophages and glomerular mesangial cells) and inducing release of inflammatory cytokines and growth factors that stimulate cellular proliferation in the glomeruli, smooth muscle of blood vessels, and collagen synthesis with fibrosis
 Induction of lipid oxidation, oxidative stress, and inflammation
 Inactivation of nitric oxide with loss of vasodilation and diminished endothelial function
 Procoagulant changes on endothelial cells with promotion of platelet adhesion and reduced fibrinolysis

A

Advanced Glycosylation End Products – AGEs

77
Q

When tissue do not require insulin for glucose transport (that is they are receiving glucose via Glut 1/2/3, then they are also using the ______ _______ which includes kidneys, RBCs, blood vessels, eye lenses, nerves, and the brain

A

Polyol Pathway

78
Q

Glucose is converted to ________ and when accumulated it increases intracellular osmotic pressure and attracts water in tissue which causes swelling

A

sorbitol

79
Q

_____interferes with ion pumps in the nerves and disrupts nerve conduction so that RBCs become swollen and stiff and interfere with perfusion

A

sorbitol

80
Q

Activation of the polyol pathway reduces ________ (an antioxidant) which contributes to oxidative injury in cells and tissues, particularly blood vessels.

A

glutathione

81
Q

______ explains:
swelling of the lenses when there is high blood sugar.
cataracts
abnormal nerve conduction
kidney changes (nephropathies of diabetes)***60-70% of all diabetes patients have it

A

Polyol Pathway

82
Q

Patho of ______ in DM:
AGEs and the increased polyols cause nerve degeneration, delayed conduction, and polyneuropathy
***especially affecting the sensory nerves

A

Neuropathies

83
Q

Thickening of the capillary basement membrane, endothelial hyperplasia, thrombosis, and pericyte degeneration r/t to glycosylation and polyol pathway and high blood glucose
***characteristic of diabetic microangiopathy

A

Microvascular Disease

84
Q

______ explains in DM:
retinopathy
nephropathy
neuropathy

A

Microvascular Disease

85
Q

• Leading cause of blindness worldwide
• Retina is the most metabolically active structure per weight of tissue in the body
o So it is a vulnerable target for neurovascular disease in DM
• Develops more rapidly in Type 2 diabetics
• Diabetics more likely to develop cataracts and glaucoma
• Macular edema (fluid accumulation and retinal thickening near the center of the macula) – leading cause of visual impairment (blurring) among persons with diabetes
• Increased risk of life-threatening systemic vascular complications, including stroke, CAD, and heart failure
• Results from relative hypoxemia, damage to retinal blood vessels and vasoconstriction, RBC and platelet aggregation, influence of vascular endothelial growth factors and growth hormone, and angiogenesis

A

Retinopathy

86
Q

• Most common cause of CKD & ESRD
• Multiple mechanisms contribute: chronic hyperglycemia, systemic hypertension, hyperperfusion, hyperfiltration, increased blood viscosity, increased glomerular pressure, albuminuria, protein kinase C, growth factors, advanced glycation end products, polyol pathway, inflammatory cytokines, oxidative stress, RAA system, hypercholesterolemia
• Glomeruli are injured by protein denaturation, hyperglycemia with high renal blood flow (hyperfiltration), and intra-glomerular hypertension resistance to glomerular capillary blood flow and decreased glomerular filtration rates (GFRs) microalbuminuria
o Microalbuminuria is the first manifestation of diabetic kidney dysfunction and develops within 5-10 years of disease

A

Nephropathy

87
Q
  • Most common complication of diabetes, affects up to 50% of people with diabetes
  • Inflammation, ischemia, oxidative stress, advanced glycation end products, and increased formation of polyol pathways contribute to demyelination, nerve degeneration, and delayed conduction
  • Occurs in both somatic and peripheral nerve cells
  • Sensory deficits usually precede motor involvement, extremities are involved first (feet then hands)
A

Neuropathy

88
Q

macrovascular changes are more often seen in DM Type __

A

1

89
Q

Complication of DM:
Unrelated to severity of DM
Contributing factors include: hyperinsulinemia (insulin resistance), hyperglycemia, hypertriglyceridemia, low levels of HDL, high levels of LDL, lipoprotein oxidation, and platelet abnormalities

A

Athersclerosis

90
Q

Complication of DM:
more prevalent in persons w/ DM than in persons w/o DM (even in persons with HTN or Hyperlipidemia) – MI and CHF
Most common cause of death for people with DMII
prevalence increases with the duration but not the severity of diabetes
HTN often coexists with DM & increases risk
In type 1- HTN is assoc with development of microalbuminuria
In type 2 – HTN is assoc with metabolic syndrome

A

Coronary Artery Disease

91
Q

Complication of DM:
 twice as common in diabetics than in non-diabetics
 more common in diabetic women
 ischemic & lacunar strokes are more common
 Risk factors: HTN, hyperglycemia, hyperlipidemia, thrombosis, and sleep apnea

A

Stroke

92
Q 
\_\_\_\_ vascular changes of DM:
Arthersclerosis
Stroke
Coronary Artery Disease
Peripheral Artery Disease
A

macro

93
Q

Complication of DM:
Increased risk with claudication, ulcers, gangrene & amputation in type 2 DM
Occlusions of the small arteries and arterioles, particularly below the knee, cause most of the gangrenous changes of the lower extremities and occur in patchy areas of the feet and toes
Risk factors: age, duration of diabetes, glycemic control, genetics, smoking, hyperlipidemia, HTN

A

Peripheral Artery/Vascular Disease

94
Q

DM patients are at higher risk for ______ due to imparied senses

A

infection

95
Q

Why Infection happens in DM:
• Once skin integrity is compromised, tissues’ susceptibility to infection increases as a result of vascular disease & hypoxia.
• Also, Glycosylated Hemoglobin in the RBCs decreases the release of oxygen to tissues

A

Hypoxia

96
Q

Why Infection happens in DM:

• proliferate more rapidly in glucose rich environment which provides excellent source of energy

A

Pathogens

97
Q

Why Infection happens in DM:

• Decreased d/t vascular changes and autonomic dysfunction, which decreases the supply of WBCs to the affected area

A

Blood Supply

98
Q

Why Infection happens in DM:
\• Chronic hyperglycemia impairs both innate and adaptive immune responses including:
o abnormal chemotaxis,
o defective phagocytosis,
o inflammatory response to infection is diminished  defective phagocytosis

A

Suppressed Immune Fxn

99
Q

Why Infection happens in DM:

• Slower collagen synthesis & decreased angiogenesis increase the opportunity for infection

A

Delayed Wound Healing

100
Q

In Hyperthyroidism (Grave’s), labs would show ____ TSH and ____ free T4

A

low; high

101
Q

TSH comes from ________

A

anterior pituitary

102
Q

T4 comes from ________

A

thyroid

103
Q

TRH comes from the _______

A

hypothalamus

104
Q

anti-TPO tests for _____ in hypothyroid patients

A

antibodies

105
Q

inflammation of the meninges, membrane that covers brain and spinal cord

A

meningitis

106
Q

where does pathogen have to go through to get to the meninges?

A

choiroid plexus

107
Q

mosquito-borne viral infection

A

encephalitis

108
Q

2 lesions in brain in Alzheimers

A

neurofibullary tangles

plaques

109
Q

seizure with stiffening of muscles and may cause one to fall to ground

A

tonic

110
Q

seizure with single or several jerks

A

myoclonic

111
Q

seizure with falling down (drop attack)

A

atonic

112
Q

seizure with jerking of many muscles and sometimes loss of bladder control (grand mal)

A

tonic-clonic

113
Q

seizure with:
o no change in level of consciousness
o Patient knows what is happening around them
o Motor, sensory, and/or autonomic symptoms present

A

focal aware (simple seizure)

114
Q

seizure with a change in the level of consciousness

A

Focal impaired awareness- (complex partial seizure)

Advanced Pathophysiology (10 decks)

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