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Advanced pathophysiology > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

Describe the etiology of Type 1 diabetes

A
  • Environmental-genetic factors are thought to trigger cell-mediated destruction of pancreatic beta cells in individuals with a genetic susceptibility
  • Autoimmune destruction of pancreatic B cells
    • Autoantibody, T-cell, and macrophage destruction
    • Causes a loss of insulin production and relative excess of glucagon
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2
Q

Describe the natural history of Type 1 diabetes

A
  • Slow progressive autoimmune T-cell-mediated disease that destroys beta cells of the pancreas
  • Gene-environment interactions result in a loss of tolerance to self-antigens with the formation of autoantigens that are expressed on the surface of pancreatic beta cells and circulate in the bloodstream/lymphatics
  • T-cytotoxic cells and macrophages are stimulated resulting in beta-cell destruction and apoptosis
  • Insulin resistance at diagnosis is unusual but may occur as the individual ages/gains weight
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3
Q

What percentage of insulin-secreting beta cells of the islet of Langerhans must be destroyed for insulin synthesis to decline enough such that hyperglycemia occurs in Type 1 diabetes?

A
  • 80% to 90%
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4
Q

Describe the pathogenesis of Type 1 diabetes

A
  • Destruction of insulin-secreting beta cells on the islet of Langerhans causes hypoinsulinemia –> This leads to a marked increase in glucagon secretion
  • Glucagon (Alpha cell hormone) that acts in the liver to increase blood glucose by stimulating glycogenolysis and gluconeogenesis
  • There is also decreased secretion of amylin (B cell hormone)
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5
Q

What contributes to hyperglycemia in type 1 DM?

A
  • Both alpha and beta-cell function are abnormal and both a lack of insulin and relative excess of glucagon contribute to hyperglycemia
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6
Q

What is the major genetic predisposition to Type 1 DM?

A
  • Appears to be conferred by diabetogenic genes of the short arm of chromosome 6, either within or in close proximity to the MHC region, or the human leukocyte antigen (HLA) region
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7
Q

Type 1 diabetes affects the metabolism of what?

A
  1. Carbohydrates
  2. Fats
  3. Proteins
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8
Q

What are the clinical manifestations of Type 1 DM?

A
  • Polydipsia ► Hyperglycemia makes the blood hypertonic and creates an osmotic pressure that sucks water out of the cells and results in intracellular dehydration and hypothalamic stimulation of thirst
  • Polyphagia ► Depletion of cellular stores of carbohydrates, fats, and proteins results in cellular starvation and increases hunger
  • Polyuria ► Hyperglycemia acts as an osmotic diuretic and glucose appears in the urine (glycosuria) as the renal threshold for glucose is exceeded and large amounts of water also lost in the urine
  • Dry mouth
  • Drowsiness
  • Stomach pain
  • Weight loss ► Is caused by the breakdown of protein and fat due to a lack of insulin for energy and because of fluid loss in osmotic diuresis
  • High levels of ketones ► Are caused by increased hepatic metabolism of fats
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9
Q

What is the best way to distinguish Type 1 DM from Type 2 DM?

A
  • Measurement of antibodies remains the best way to identify diabetes and distinguish Type 1 DM from other types
    • Having 2 or more islet autoantibodies confers a 100% risk of diabetes development
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10
Q

Describe the etiology of Type 2 DM

A
  • Results from insulin resistance ► Glucose is then unable to enter the cells
    • Insulin binds to cell surface receptors, however
      • The binding may be impaired
      • There may be fewer receptors
      • There may be post-receptor defects

OR

  • A defect in pancreatic B-cell secretion
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11
Q

Describe the natural history of Type 2 DM

A
  • Stage 1
    • Increased insulin present
    • Genetic/environmental factors present
    • Cause insulin resistance
    • Hyperinsulinemia ensues → Insulin overdrive to overcome insulin resistance
    • Temporary restoration of normal blood glucose
  • Stage 2
    • Decreased suppression of visceral fat lipolysis
    • Increase in free fatty acids
    • Insulin resistance increases
    • Results in impairment in glucose uptake in insulin-sensitive tissues (primarily in muscles)
    • Hyperinsulinemia ensues
    • B cells are exhausted due to increased insulin demands and develop a secretory defect
    • Results in postprandial hyperglycemia with normal fasting blood glucose
  • Stage 3
    • Increase in free fatty acids
    • Increased insulin resistance
    • Hyperinsulinemia
    • Causes suppression of hepatic glucose production
    • Fasting and postprandial hyperglycemia
    • Downregulation of insulin receptors and impairment of post-receptor events
    • Leading to more hyperglycemia which is toxic to B cells
    • B cells produce LESS insulin
    • Leads to type 2 DM
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12
Q

List the most well-recognized risk factors for the development of Type 2 DM

A
  • Age
  • Obesity
  • HTN
  • Physical inactivity
  • Family hx
  • Metabolic syndrome
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13
Q

List the response of the following organ/body system in Type 2 DM:

  1. Liver
  2. Pancreas
  3. Peripheral tissue (muscle)
A
  1. Liver ⇒ Increases glucose production despite an overall increase of glucose already in the body
  2. Pancreas ⇒ Impaired insulin secretion
  3. Peripheral tissue ⇒ Glucose is unable to enter, so not enough glucose is entering the cells
    • Peripheral tissues resistant & so increased insulin secretion is result
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14
Q

Pathophysiology of Type 2 DM

A
  • Caused by genetic susceptibility that is triggered by environmental factors
    • The most compelling environmental risk factor is OBESITY
  • Insulin production continues but the weight and number of beta cells decrease
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15
Q

What are the clinical manifestations of Type 2 DM?

A
  • Nonspecific symptoms…
    • Fatigue
    • Pruritus
    • Recurrent infections
    • Prolonged wound healing
    • Visual changes
    • Symptoms of neuropathy
    • Parasthesias
    • Acanthosis nigricans (brown/black pigmentation in body folds associated with insulin resistance)
    • Obesity
    • Dyslipidemia
    • Hypertensive
    • Hyperinsulinemic
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16
Q

The diagnosis of DM is based on what?

A
  • HgbA1C: > 6.5%

OR

  • FPG:> 126 mg/dL (fasting=no caloric intake for at least 8 hrs)

OR

  • 2-hr plasma glucose:> 200 mg/dL during an OGTT

OR

  • In a patient with classic symptoms of a hyper/hypoglycemia crisis and a random plasma glucose _>_200 mg/dL
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17
Q

Define insulin resistance

A
  • A suboptimal response of insulin-sensitive tissues (especially the liver, muscle, and adipose tissue) to insulin and is associated with obesity
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18
Q

What are the mechanisms that contribute to insulin resistance?

A
  • Abnormality of the insulin molecule
  • High amounts of insulin antagonists
  • Downregulation of the insulin receptor
  • Decreased or abnormal activation of postreceptor kinases
  • Alteration of glucose transporter genes (GLUT)
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19
Q

Islet dysfunction of B cells in response to prolonged hyperinsulinemia is caused by a combination of what?

A
  • A decrease in beta-cell mass
  • A reduction in beta-cell function
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20
Q

Why is glucagon concentration increased in Type 2 DM?

A
  • Pancreatic alpha cells become less responsive to glucose inhibition⇒ Results in increased glucagon secretion
  • Increased glucagon causes an increase in blood glucose levels by stimulating glycogenolysis (the breakdown of glucose as it enters the cell) and gluconeogenesis (creating glucose from nonglucose sources-i.e., liver)
  • Amylin deficiency also increases glucagon secretion/hyperglycemia
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21
Q

What is ghrelin and how is it associated to insulin resistance?

A
  • It is a peptide produced in the stomach and pancreatic islets that regulate food intake, energy balance, and hormonal secretion
  • Decreased levels associated with insulin resistance and increased fasting insulin levels
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22
Q

What are incretins and how are they related to insulin resistance?

A
  • A class of peptides that are released from the GI tract in response to food intake and function to increase synthesis and secretion of insulin and beta-cell proliferation and protect against beta-cell damage
  • Beta-cell responsiveness to GLP-1 is reduced in Type 2 DM and prediabetes
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23
Q

How does obesity contribute to insulin resistance and diabetes (5 mechanisms)?

A
  1. Alteration in the production of adipokines by adipose tissue (i.e., leptin resistance) ⇒ Decreased insulin synthesis and insulin resistance
  2. Elevated levels of serum-free fatty acids and intracellular lipid deposits ⇒ Interfere with intracellular insulin signaling, decrease tissue response to insulin, alter incretion action, promote inflammation, and cause apoptotic beta-cell death (lipotoxicity)
    * 3.* Release of inflammatory cytokines from adipose tissue ⇒ Induce insulin resistance through a post-receptor mechanism
  3. Reduced insulin-stimulated mitochondrial activity and insulin resistance
  4. Obesity-associated insulin resistance ⇒ Correlated with hyperinsulinemia and impaired insulin receptor signaling
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24
Q

List the three general mechanisms of insulin resistance

A
  • Decreased amylin and ghrelin levels and decreased beta-cell response to glucagon-like peptides are associated with insulin resistance/Type 2 DM
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25
Q

What does a glycosylated hemoglobin level measure?

A
  • Reflects the average blood sugar level over 90-120 days
    • What percentage of Hgb has been exposed to sugar and how much sugar
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26
Q

What is the Hgb A1C test used for?

A
  • Identify prediabetes
  • Diagnose Type 1 and Type 2 DM (will perform two separate tests on different dates to confirm)
  • Monitor current diabetes treatment plan
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27
Q

HgbA1C levels

A

► Normal A1C <5.7%

►Prediabetes AIC _>_5.7% and <6.5%

►Diabetes AIC >6.5%

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28
Q

What are impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) caused by?

A
  • IGT is caused by diminished insulin secretion
  • IFG is caused by enhanced hepatic glucose output secondary to hepatic insulin resistance
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29
Q

What levels of fasting plasma glucose (FPG) demonstrate impaired fasting glucose (IFG) seen in prediabetes?

A
  • FPG: 100-125 mg/dl
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30
Q

2-hr plasma glucose level during oral glucose tolerance testing (OGTT) (using a 75-g PO glucose load) demonstrating impaired glucose tolerance (IGT) seen in prediabetes?

A
  • 140-199 mg/dl
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31
Q

HgbA1c level demonstrating prediabetes

A
  • 5.7-6.4%
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32
Q

List the chronic microvascular complication of DM

A
  • Damage to the capillaries, including:
    • Retinopathy
    • Neuropathy
    • Nephropathy
    • Amputations
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33
Q

List the chronic macrovascular complications of DM

A
  • Damage to the larger vessels, including:
    • CAD
    • Stroke
    • Peripheral vascular and cerebral vascular disease
34
Q

Describe the causes of chronic diseases in DM

A
  • Chronic complications are caused by:
    • Insulin resistance/deficiency
    • Chronic hyperglycemia
    • Accumulation of advanced glycation end-products
    • Activation of metabolic pathways that cause tissue damage
35
Q

What are the tissues that do NOT require insulin for glucose transport and how does this impact the development of chronic conditions?

A
  • Tissues that are unable to downregulate the cellular uptake of glucose:
    • Kidneys
    • RBCs
    • Blood vessels
    • Eye lens
    • Nerves
  • Metabolic complications affect these tissues then and result in complications. These include:
    • Oxidative stress
    • Sunting of glucose to the polyol pathway
    • Activation of protein kinase C
    • Formation of AGEs
    • Accumulation of hexosamines
36
Q

Microvascular complications in diabetes

A
  • The leading cause of blindness, end-stage kidney failure, and various neuropathies
  • Characteristics of diabetic microangiopathy include:
    • Occlusion of capillaries with thicking of the capillary basement membrane
    • Endothelial cell hyperplasia
    • Thrombosis
    • Pericyte degeneration
    • Hypoxia/ischemia
37
Q

Causes of diabetic retinopathy

A
  • Develops more rapidly in type 2 DM d/t longstanding hyperglycemia before diagnosis
  • Comorbid diseases include cataracts and glaucoma
  • Results from:
    • Damage to retinal blood vessels and red blood cells, p
    • Platelet aggregation
    • Relative hypoxemia & HTN
38
Q

List and describe the three stages of diabetic retinopathy that lead to loss of vision

A
  • Stage 1: Nonproliferative
    • Macular edema ⇒ The leading cause of visual impairment/blurring in DM
    • Vein abnormalities
    • Microaneurysm formation
    • Interretinal hemorrhage
    • Hard exudates
  • Stage 2: Preproliferative
    • Cotton-wool patches (d/t retinal ischemia)
    • Intraretinal microvascular shunts
  • Stage 3: Proliferative
    • Neovascularization
    • Glial proliferation
    • Vitreoretinal traction hemorrhage; retinal detachment
39
Q

Describe the causes of diabetic kidney disease

A
  • Hyperglycemia activates the polyol pathway, hexosamine pathway, protein kinase C, production of advanced glycation end-products (AGEs), and inflammation ⇒ These all contribute to kidney tissue injury
  • Changes include:
    • Glomerular enlargement
    • Glomerular basement membrane thickening w/proliferation of mesangial cells
    • Proliferation of mesangial matrix
40
Q

Clinical manifestations of diabetic kidney disease

A
  • Kimmelstiel-Wilson nodule (nodular glomerulosclerosis)
  • Podocyte loss
  • Decreased GFR
  • Microalbuminuria (30 to 300 mg/day) ► First manifestation of kidney dysfunction
    • ​Seen often in Type 1 DM
  • Later we may see…
    • Fluid overload
    • Hypoproteinemia
    • Decreased plasma oncotic pressure
    • Anasarca (generalized body edema)
    • HTN
  • Macroalbuminuria (>300 mg/day)
41
Q

Describe the general etiology of diabetic neuropathies

A
  • Since nerves do not require insulin for glucose transport, they are vulnerable to chronic hyperglycemia*
  • More common in Type 2 DM
  • The underlying pathologic mechanism includes both: Metabolic and vascular factors r/t chronic hyperglycemia with…
    • Inflammation
    • Ischemia
    • xidative stress
    • Advanced glycation end-products
    • Increased polyol formation ⇒ demyelination
    • Nerve degeneration
42
Q

Describe the clinical manifestations of diabetic neuropathies

A
  • Nerve degeneration begins in the peripheral
  • Sensory deficits proceed motor involvement
  • Extremities involve first!!
    • “Stocking and glove” pattern
43
Q

Describe distal symmetric polyneuropathy

A
  • Most common neuropathy and involves both small and large nerve fibers
    • Sensory, autonomic, and motor nerve involvement
  • Loss of small nerve fiber function ► Causes neuropathic pain and sensation loss, high risk of foot ulceration development, gangrene and amputation risk
  • Loss of large nerve fiber function ► Causes sensory loss of proprioception and vibration, ataxia, loss of coordination, the risk for falls/fractures
  • Motor weakness, muscle atrophy seen later in the disease of lower legs/feet
44
Q

Describe autonomic neuropathies

A
  • Affect GI enteric nerves causing:
    • Nausea, bloating, diarrhea, gastroparesis, or constipation
    • Bladder/sexual dysfunction
      • Urinary retention, loss of bladder sensation, recurrent infection, erectile dysfunction
    • Cardiovascular autonomic neuropathy is a serious complication
      • HR variability, changes in baroreceptor reflexes, postural hypotension, dysrhythmias, painless MI, sudden death
45
Q

Describe Charcot neuroarthropathy (Charcot joint)

A
  • The progressive degeneration and structural disorganization of a joint, particularly in the foot or ankle in long-term DM
  • Is related to inflammation, loss of sensation, and neurally mediated vascular alteration with osteoclastic bone reabsorption
46
Q

Describe diabetic microvascular disease

A
  • Lesions in large and medium-sized arteries
  • Increases risk for HTN, accelerated atherosclerosis, hyperlipidemia, CVD, stroke, and peripheral vascular disease
  • Unrelated to the severity of DM unlike microangiopathy**
  • Found in those with insulin resistance and impaired glucose tolerance
47
Q

Describe CVD in relation to DM

A
  • Ultimate cause of death in DM
  • Type 1 DM: HTN is associated with the development of microalbuminuria
  • Type 2 DM: HTN is associated with metabolic syndrome
  • HTN increased risk for CAD and stroke
    • CAD prevalence increases with the duration but not the severity of DM
    • CAD and stroke in DM are the consequence of accelerated atherosclerosis, HTN, and increased risk for thrombus formation
48
Q

Describe peripheral artery disease in DM

A
  • Is an atherosclerotic disease of the lower extremity and DM increases the incidence of PAD
  • Development is nfluenced by age, duration of diabetes, glycemic control, and smoking, hyperlipidemia, and HTN
49
Q

Describe the clinical manifestations of peripheral artery disease

A
  • Pain from reduced blood flow (claudication)
  • Ulcers
  • Gangrene –> Results in amputation
    • Results from occlusion of small arteries and arterioles
    • Occur in patchy areas to feet/toes
    • Begin as ulcers and progress to osteomyelitis or gangrene and require amputation
50
Q

Describe the causes of hypoglycemia

A
  • Occurs when blood glucose levels are less than 47 mg/dL in newborns for the first 48 hrs of life OR less than 70 mg/dL in children and adults
  • Occurs when blood glucose levels are low enough to cause epinephrine secretion resulting in the “flight or fight response”
    • Either there is excess insulin or decreased counter-regulatory hormones
  • Causes may be:
    • ​Exogenous ► Meds, EtOH, exercise
    • Endogenous ► Tumors of the pancreas or inherited DO’s
    • Functional ► Hyperalimentation, spontaneous, or liver disease
  • Type 2 DM is less of a risk for hypoglycemia than Type 1
  • Associated with insulin or oral medication use
51
Q

List the precipitating factors in hypoglycemia

A
  • Insulin-treated patients
  • Selected PO hypoglycemic meds
  • Combo med/insulin therapy
  • Incorrect dose of meds
  • Decreased caloric intake
  • Skipping meals/snacks
  • Exercise or increased physical activity without adequate food intake
52
Q

Physiologic responses to hypoglycemia in individuals without DM

A
  • Blood glucose levels decrease
  • In return, insulin levels appropriately decrease as well
  • Glucagon and other counter-regulatory hormones increase from the liver
  • Glucose level increases
53
Q

Physiologic response to hypoglycemia in individuals with DM treated with insulin or PO meds

A
  • Blood glucose levels decrease
  • Insulin levels appropriately decrease
  • Glucagon and other hormones increase, but the response is not enough
  • Glucose levels do not sufficiently increase and patient remains hypoglycemia
54
Q

What are the clinical manifestations of hypoglycemia?

A
  • Adrenergic reactions (Autonomic): Occur when decrease in glucose level is rapid
    • Pallor
    • Sweating
    • Tachy/palpitations
    • Hunger
    • restlessness
    • Anxiety/tremors
  • Neurogenic reactions (Neuroglycopenic):
    • Fatigue
    • Irritability
    • Headache
    • Loss of concentration
    • Confusion
    • Transient sensory/motor defects
    • Convulsions
    • Coma/death
55
Q

What is hypoglycemia unawareness?

A
  • When an individual with hypoglycemia lacks appropriate autonomic warning signs and recovery may be delayed because of impaired glycogenolysis and hampered delivery of gluconeogenic substrates the liver
  • Autonomic symptoms not felt due to impaired glucagon response
    • Glucagon doesn’t rise and is sluggish in responding to hyperglycemia
  • Huge problem with Type 1 DM
  • Treatment: Lighten up on tight glucose control
56
Q

Describe the pathophysiology of DKA

A
  • There is increased lipolysis and triglyceride breakdown
    • Body is digesting its fats
  • There’s also decreased glucose uptake
    • So the body is taking up less glucose and there’s increasing breaking down of proteins
  • In addition, there is increased free fatty acids which in turn leads to ketogenesis
    • increased formation of ketones which will, in turn, lead to acidosis
  • Increased free fatty acids also lead to hyperglycemia, as will decreased glucose uptake
    • Hyperglycemia leads to increased glucose in the urine which will, in turn, lead to more urine production ► Osmotic diuresis
      • Osmotic diuresis leads to volume depletion and electrolyte loss as well
    • May lead to impaired renal function which can worsen acidosis
  • Also have increasing proteolysis and increasing amounts of breaking down of the proteins
    • Lead to increased amino acids, and then increased gluconeogenesis
  • The body responds by making more glucose which will, in turn, lead to worsening hyperglycemia and increasing osmotic diuresis
  • Cellular dehydration leads to a loss of K from cells and a net loss of body K
  • OVERALL…DKA is r/t a deficiency of insulin and an increase in the levels of insulin counter-regulatory hormones (catecholamines, cortisol, glucagon, growth hormone)
57
Q

What are the clinical manifestations of DKA?

A
  • Weakness
  • Blurry vision
  • Abdominal pain *
  • Nausea/vomiting
  • Altered mental status
  • Kussmaul respirations
  • Hyperventilation d/t acidosis
  • Hypotension
  • Tachycardia
  • Ketone smelling breath
  • Elevated blood sugar usually above 250
  • Serum ketones > 15 (ketonuria)
  • Anion gap metabolic acidosis
  • Polyuria and dehydration due to osmotic dehydration r/t hyperglycemia
    • ​Plasma glucose level is higher than the renal threshold, so significant amounts of glucose is lost in the urine
  • ​Deficits in NA, phosphorous and Mg
  • Decreased total body K!! (level may appear normal/elevated)
58
Q

What do you give to a patient experiencing DKA to correct the metabolic acidosis?

A
  • Give insulin ⇒ Watch for K level drop!!! Give supplemental K as well
59
Q

What are the 4 end-points of DKA?

A
  1. Dehydration
  2. Fluid/electrolyte loss
  3. Metabolic acidosis
  4. Hyperglycemia
60
Q

List the risk factors for DKA

A
  • Occurs in approx. 30 % of children with Type 1 DM
  • More common in Type 1 d/t increased insulin deficiency
  • Obesity
  • Non-Hispanic black ethnicity
  • Intercurrent illness ** (infection, trauma, surgery, or MI)
  • Poor med compliance and/or interruption of med treatment
  • Poor glycemic control
  • Younger or older age
  • Diagnostic error
  • Lack of health insurance in the US
  • Lower body mass index
61
Q

List the diagnostic criteria for DKA

A
  1. Serum glucose >250 mg/dL
  2. Serum bicarb level <18
  3. Serum pH <7.30
  4. Presence of an anion gap
  5. Presence of urine and serum ketones
62
Q

How does HHS differ from DKA?

A
  • In the degree of insulin deficiency (more profound in DKA) and the elevation of glucose levels and degree of fluid deficiency (more profound in HHS)
  • HHS develops over time, where DKA has more of a rapid onset
63
Q

Describe the pathophysiology of DKA

A
  • Insulin deficiency and increased levels of counter-regulatory/stress hormones (glucagon, catecholamines, cortisol, and growth hormone)
    • Insulin levels sufficient though to prevent excessive lipolysis but not to use glucose properly
  • Increased gluconeogenesis, and glycogenolysis
  • Inadequate use of peripheral tissues, primarily muscle
  • Lack of ketosis
64
Q

What are the risk factors for developing HHS?

A
  • Type 2 DM
  • Elderly
  • Comorbid issues (infections, renal, or cardiac disease)
  • Massive fluid loss
65
Q

List the clinical manifestations of HHS

A
  • Glycosuria
  • Polyuria
  • Extreme serum glucose elevation
  • Severe volume depletion
  • Increased serum osmolality (up to 400)
  • Intracellular dehydration
  • Electrolyte loss (including K)
  • Neurologic changes (stupor)
66
Q

List the diagnostic criteria for HHS

A
  1. Very high serum glucose (usually > 600 mg/dL)
  2. Near normal sodium bicarb and pH
  3. A serum osmolarity usually > 320 mOsm/L
  4. Absent or low ketones in the urine/serum
67
Q

Describe the etiology of hyperthyroidism

A
  • When excess amounts of TH are secreted from the thyroid gland
  • Primary causes include:
    • Grave’s disease
    • Toxic multinodular goiter
    • Thyroid adenoma
    • Thyroiditis
  • Secondary causes include:
    • TSH-secreting pituitary adenomas
68
Q

Describe the pathophysiology of Grave’s Disease

A
  • Exact cause is unknown
  • Thought to be genetic factors interacting with environmental triggers
  • Is an autoimmune disease that results from stimulation of the thyroid by thyroid-stimulating immunoglobulins (TSI’s)
    • TSI’s override the normal negative feedback mechanisms and causes an increased synthesis of TH and hyperplasia of the gland (goiter)
  • TRH and TSH decrease
69
Q

Describe the risk factors for Grave’s Disease

A
  • More common in women
  • Familial predisposition of approx. 15%
  • Occurs at any age, but peak onset is 20-40 years
70
Q

Describe the clinical manifestations of Grave’s Disease

A
  • Ophthalmopathy
    • Lag of the globe on upward gaze or lag of the upper lid on downward gaze
  • Dermopathy
    • Only with very high TSI levels
    • Subcutaneous swelling on the anterior portions of the legs and by indurated and erythematous skin
  • Exophthalmos (protrusion of the eyeballs)
  • Double vision
  • Periorbital edema
  • Decreased visual acuity
71
Q

List the diagnostic criteria of Grave’s Disease

A
  • Hyperthyroidism
  • Diffuse goiter (smooth and soft)
  • Ophthalmopathy (exophthalmos)
  • Dermopathy
72
Q

What are the clinical manifestations of hyperthyroidism?

A
  • Endocrine
    • Enlarged thyroid gland (goiter)
    • Bruit heard over thyroid
    • Hypercalcemia
    • Decreased PTH secretion
  • Reproductive
    • Erectile dysfunction
    • Decreased libido
    • Menstrual abnormalities
  • GI
    • Weight loss
    • Nausea/vomiting
    • Anorexia
    • Abdominal pain
  • Integumentary
    • Warm skin with a velvety texture
    • Heat intolerance
    • Sweating
    • Hair that is fine and soft
    • Palmar erythema
    • Occasionally vitiligo
    • Hair loss
  • Eyes
    • Prominent stare
    • Lid lag
    • Failure of convergence
    • Failure to wrinkle brow on upward gaze
  • Cardiovascular
    • Tachycardia
    • Palpitations
    • Wide pulse pressure
    • Arrhythmias (i.e., elderly with atrial fibrillation)
    • Systolic murmors
  • Neurologic
    • Tremor
    • Hyperreflexia
    • Emotional lability
73
Q

What is a complication of hyperthyroidism?

A
  • Thyroid storm
    • Worsening of the hyperthyroid state
    • Death can occur within 48 hours without treatment
    • Typically occurs in individuals with undiagnosed or partially treated severe hyperthyroidism and who are subject to excessive stress
      • I.e., infection, cardiovascular disorders, trauma, burns, seizures, surgery
    • Symptoms are caused by the sudden release and increased action of thyroxine (T4) and triiodothyronine (T3) exceeding metabolic demands
      • Hyperthermia
      • Tachycardia (atrial dysrhythmia)
      • High-output HF
      • Agitation/delirium
      • Nausea/vomiting/diarrhea
      • Fluid volume depletion
74
Q

List the laboratory findings associated with hyperthyroidism

A
  • Primary hyperthyroidism:
    • Decreased TSH
    • Elevated T3 and T3 uptake
    • Decreased T4
    • Elevated serum TA
  • Secondary hyperthyroidism:
    • ​Normal to increased TSH
    • Elevated TH
75
Q

Describe the etiology of hypothyroidism

A
  • Congenital defects
  • Idiopathic
  • Past radioactive iodine surgery or irradiation
  • Biosynthetic defects
  • Drugs (i.e., Lithium!)
  • Iodine deficiency
  • Chronic thyroiditis (Hashimoto’s thyroiditis)
  • Transient phase of subacute thyroiditis
76
Q

How is radioactive iodine used to differentiate the different types of hyperthyroidism?

A
  • Radioactive uptake with thyroid suppression test in increased
  • Grave’s Disease
    • A pattern of iodine uptake will show a diffuse and concentrated uptake occurring quickly
  • Toxic Multinodular Goiter
    • Iodine uptake will show in certain spots and there will be suppressed areas around
  • Thyroid Adenoma
    • Iodine uptake will show TH release concentrated to one area and suppression in the other surrounding areas
77
Q

Describe the pathophysiology of hypothyroidism

A
  • Primary hypothyroidism
    • Leads to a decreased production of TH and an increased secretion of TSH and TRH
    • Most common cause ⇒ Autoimmune thyroiditis (Hashimoto’s)
      • Head and neck radiation therapy
      • Endemic iodine deficiency
  • Central hypothyroidism
    • Caused by the pituitary’s failure to synthesize adequate amounts of TSH or lack of TRH
78
Q

Describe Hashimoto’s disease

A
  • Most common cause of hypothyroidism and is an autoimmune disorder
    • Antimicrosomal antibodies present in 85% of cases
  • More common in women
  • Most sig. clinical feature is a goiter
  • Diagnosed by the presence of thyroperoxidase and thyroglobulin antibodies
79
Q

List the clinical manifestations of hypothyroidism

A
  • Neurological
    • Confusion
    • Lethargy
    • Slow/clumsy movements
    • Hearing loss
    • Night blindness
  • Endocrine
    • Increased TSH in primary hypothyroidism
  • Reproductive
    • ​Decreased androgen secretion in men
    • Increased estriol in women
  • Hematologic
    • Decreased RBC mass → Normochromatic anemia
    • Vitamine B12 deficiency and inadequate folate/iron absorption
  • Cardiovascular
    • Reduction in stroke volume and HR causing a decreased cardiac output
    • Cardiomegaly
    • Cool skin
    • Cold intolerance
  • Renal
    • Reduced renal blood flow and GFR leading to decreased renal water secretion
  • GI
    • Constipation
    • Weight gain
    • Fluid retention
    • Edema
    • Decreased glucose absorption and delayed glucose uptake
  • Musculoskeletal
    • The prolonged relaxation phase of deep tendon reflexes
    • General weakness
    • Lethargy
    • Arthralgias
  • Integumentary
    • Dry hair with the tendency for it to fall out
    • Cool, tough doughy skin
    • Myxedema
    • Slow wound healing
    • Flat face
80
Q

What is a complication of hypothyroidism?

A
  • Myxedema coma ⇒ A diminished level of consciousness associated w/severe hypothyroidism
    • Usually not conscious
    • Precipitating factors → Infections, discontinued thyroid supplements, narcotic or sedative overuse consequence of acute illness
    • Risk factors → Older individuals w/comorbid conditions
    • S/S’s → Hypothermia w/o shivering, hypoventilation, hypotension, hypoglycemia, lactic acidosis, and coma
81
Q

List the laboratory value findings for hypothyroidism

A
  • Primary hypothyroidism:
    • Increased TSH and TRH
    • Decreased TH
    • Decreased T3 and T4
    • Hyponatremia
  • Secondary hypothyroidism:
    • ​Pituitary malfunction:
      • ​​Low levels of TSH and TH
      • Increased TRH
    • Hypothalamic malfunctions:
      • ​Low levels of TRH, TSH, and TH

Advanced pathophysiology (3 decks)

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