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From Flashcardlet > Patho - summer exam 2 > Flashcards

Patho - summer exam 2 Flashcards

1
Q

What is the general age of onset for primary PD?

A

>40 years of age

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2
Q

What kind of medications can cause secondary PD?

A

Dopamine antagonists

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3
Q

What are some of the theories behind the etiology of PD?

A
  • Vascular problems in the brainstem
  • Viral
  • Metabolic
  • Increased microglial activity leading to increased free radicals
  • Increased glutamate activity leading to increased calcium
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4
Q

What are some environmental factors found to be protective against PD?

A
  • Nicotine
  • Anti-inflammatories
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5
Q

What will result if a person has synuclein missense mutations?

A

The mutations are an autosomal dominant cause of early-onset PD

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6
Q

What is the gold standard for diagnosing PD?

A

Neuropathy on autopsy

  • Depigmentation in substantia nigra
  • Neuronal loss in substantia nigra
  • Lewy bodies
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7
Q

How does one actually go about diagnosing PD?

A

Based on clinical manifestations

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8
Q

What clinical manifestations must be present to diagnose PD?

A

At least 2 of the following:

  • Tremor (resting)
  • Rigidity (cogwheel)
  • Akinesia
  • Postural instability
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9
Q

What are some of the cardinal physical exam findings with a PD patient?

A
  • lack of convergence to penlight
  • exaggerated glabellar tap reflex
  • blepharoclonus
  • head drop/rigidity
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10
Q

Why do you need to monitor cardiovascular status when a patient is on an MAO-I or COMT-I?

A

Dopamine is broken down by hydroxylase to NE, which is broken down by transferase to Epi… Dopamine is increased in people on these meds

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11
Q

What side effects are associated with dopamine agonists?

A

Psychosis, hallucinations

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12
Q

How would you treat a patient >60 years old for PD?

A
  • Use Sinemet, can add a dopamine agonist
  • Avoid selegiline, amantadine, anticholinergics
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13
Q

How would you treat a patient 50-59 years old for PD?

A
  • Use selegiline or a dopamine agonist
  • Can add Sinemet or amantadine
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14
Q

How would you treat a patient <50 years old for PD?

A
  • Use selegiline, amantadine, anticholinergics
  • Avoid Sinemet, l-dopa
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15
Q

What adverse effect could occur with a bilateral thalmotomy?

A

Dysarthria

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16
Q

What are some risk factors for the development of Schizophrenia?

A
  • Family history
  • Living in an urban area
  • Immigration
  • Obstetric complications during pregnancy or delivery
  • Influenza virus exposure with late winter/early spring birth
  • Advanced paternal age at conception
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17
Q

What are some of the positive symptoms associated with Schizophrenia?

A
  • Hallucinations
  • Delusions
  • Disorganized and inappropriate behavior
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18
Q

What are some of the negative symptoms associated with Schizophrenia?

A
  • Affective disorder
  • Alogia
  • Apathy
  • Anhedonia/Asociality
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19
Q

What are some metabolic disturbances associated with schizophrenia and medications that treat it?

A
  • Diabetes
  • Hyperlipidemia
  • Hypertension
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20
Q

On what type of schizophrenia symptoms does first generation psychotics work best?

A

Positive symptoms

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21
Q

On what type of schizophrenia symptoms does second generation psychotics work the best?

A

Positive AND negative symptoms

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22
Q

What type of physical alterations are found in the brains of individuals with schizophrenia?

A
  • Enlarged lateral and third ventricles
  • Widened frontal cortical fissures and sulci
  • Increased rate of cortical gray matter loss, especially in individuals not taking medication
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23
Q

What is the function of D1 receptors (D1 and D5)?

A

Activation of adenylyl cyclase, can produce bipolar disease

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24
Q

What is the function of D2 receptors (D2, D3, and D4)?

A

Inhibition of adenylyl cyclase

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25
Q

What is the result of overactive D2 receptors?

A

Schizophrenia

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26
Q

What is the result of inactive D2 receptors?

A

Recurrent major depression

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27
Q

What type of schizophrenia symptoms results from upregulation of the mesolimbic pathway?

A

Positive symptoms

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28
Q

What type of schizophrenia symptoms results from dysfunction of the mesocortical pathway?

A

Negative symptoms

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29
Q

In what two areas of the brain are high concentrations of dopaminergic neurons located?

A
  • Substantia nigra
  • Ventral tegmental area (VTA)
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30
Q

What are some side effects of the typical antipsychotics (dopamine antagonists)?

A
  • extrapyramidal symptoms (PD-like)
  • hyperprolactinemia (lactation, sexual dysfunction)
  • tardive dyskinesia
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31
Q

What are some side effects of the atypical antipsychotics?

A
  • Weight gain
  • Agranulocytosis (in 10%)
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32
Q

What are two types of neuroendocrine dysregulation that you need to rule out before diagnosing major depressive disorder?

A
  • Hypothalamic-pituitary-adrenal system dysregulation (altered cortisol production)
  • Hypothalamic-pituitary-thyroid system dysregulation (hypothyroidism)
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33
Q

In what key way do the TCAs vary?

A

TCAs vary in their ability to block the reuptake of the various neurotransmitters (serotonin, NE, and dopamine)… If one doesn’t work well, switch to one that affects another neurotransmitter better

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34
Q

What are the zymogens secreted by pancreatic acinar cells?

A
  • Trypsinogen
  • Chymotrypsinogen
  • Procarboxypeptidase A & B
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35
Q

What are the predominant cells in the pancreatic islet?

A

Beta cells make up ~60% of islet cells

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36
Q

Why is it important to decrease the dose of insulin for a patient with liver disease?

A

The patient will not be able to produce an adequate amount of insulinase, an enzyme produced by the liver to degrade insulin

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37
Q

How do sulfonylureas increase the release of insulin?

A

Sulfonylureas block the K+ transporter to trap K+ inside the beta cells, resulting in depolarization and insulin release

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38
Q

How do GLUT-2 transport inhibitors treat diabetes?

A

By inhibiting the GLUT-2 receptors in the proximal kidney, they allow the patient to spill glucose into the urine instead of reabsorbing it

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39
Q

What is a contraindication for GLUT-2 transport inhibitors?

A

Renal failure

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40
Q

What processes are stimulated by insulin secretion in muscle cells?

A
  • Glycogenesis
  • Lipogenesis
  • Protein synthesis
41
Q

What processes are inhibited by insulin secretion in muscle cells?

A
  • Gluconeogenesis
  • Glycogenolysis
  • Ketogenesis
  • Proteolysis
42
Q

What liver processes are stimulated by insulin secretion?

A
  • Glycogenesis
  • Lipogenesis
  • Protein synthesis
43
Q

What liver processes are inhibited by insulin secretion?

A
  • Gluconeogenesis
  • Glycogenolysis
  • Ketogenesis
44
Q

What adipose processes are stimulated by insulin secretion?

A

Lipogenesis

45
Q

What adipose processes are inhibited by insulin secretion?

A

Ketogenesis

46
Q

At what plasma glucose level is the maximum amount of insulin secreted?

A

When plasma glucose is approximately 200 mg/dL

47
Q

What are some factors that stimulate insulin secretion?

A
  • Glucose
  • Amino acids
  • Free fatty acids
  • GI hormones (GLP-1, GIP, secretin)
  • PNS stimulation
  • SNS via beta adrenergic receptors
48
Q

What are some factors that inhibit insulin secretion?

A
  • Fasting
  • Exercise
  • SNS via alpha adrenergic receptors
49
Q

Why must you use caution when prescribing a beta blocker to a type II diabetic?

A

Blocking the beta receptors prevents the stimulation of insulin release via that mechanism… monitor the blood sugar response frequently in these cases

50
Q

What are the effects of glucagon secretion?

A
  • Increased plasma glucose
  • Increased plasma free fatty acids
  • Increased plasma ketoacids
  • Decreased plasma amino acids
51
Q

Why does beta adrenergic stimulation stimulate insulin AND glucagon secretion?

A

If only insulin was released in a fight or flight situation, it would result in decreased blood glucose, which would not be beneficial. Stimulating the secretion of glucagon increases blood glucose in an attempt to keep glucose in a normal range.

52
Q

Why do increased amino acids stimulate the secretion of insulin AND glucagon?

A

If only insulin was secreted after a high protein meal with no carbohydrates, blood glucose would bottom out. Stimulation the secretion of glucagon as well protects the brain so it can get enough glucose in these situations.

53
Q

What are some factors that stimulate glucagon secretion?

A
  • Hypoglycemia
  • Fasting
  • Exercise
  • Amino acids
  • SNS via beta adrenergic receptors
  • CCK and gastrin
54
Q

What are some factors that inhibit glucagon secretion?

A
  • Glucose
  • Insulin
  • Free fatty acids
  • Ketoacids
  • SNS via alpha adrenergic receptors
55
Q

At what plasma glucose level does glucagon secretion begin to increase?

A

When plasma glucose decreases to around 80 mg/dL

56
Q

What test is more sensitive at picking up type II DM: fasting plasma glulcose or oral glucose tolerance?

A

OGTT

57
Q

What characteristic of type 2 diabetics makes them less prone to ketoacidosis as type 1 diabetics?

A

Endogenous insulin production in type 2 diabetics prevents the breakdown of fat

58
Q

What are other types of diabetes besides DM types 1 and 2?

A
  • Maturity onset diabetes of the young (MODY)
  • Neonatal diabetes
  • Maternally inherited diabetes and deafness
  • Gestational diabetes
59
Q

What fraction of women with gestational diabetes develop type 2 DM immediately following pregnancy?

A

1/3

60
Q

When do type 1 DM symptoms begin to manifest?

A

When 90% or more of the beta cells are destroyed

61
Q

What symptoms do type 1 diabetics usually present with?

A

Polyuria, polydipsia, polyphagia

62
Q

What symptoms do type 2 diabetics usually present with?

A

Most are asymptomatic or present with nonspecific symptoms

63
Q

What are some reasons why people with diabetes are at increased risk for infection?

A
  • Impaired senses
  • Tissue hypoxia
  • Pathogens proliferate well in glucose
  • Decreased delivery of WBCs
  • Altered WBC function
64
Q

What are some of the macrovascular complications of DM?

A

CAD and CVA

65
Q

What are some of the microvascular complications of DM?

A
  • Nephropathy
  • Retinopathy
  • Neuropathy
66
Q

Why can newborns tolerate lower blood glucose than children and adults?

A

Newborns can use sources other than glucose as substrates for their neurons

67
Q

How will manifestations of hypoglycemia change in a patient on beta blockers?

A

A patient on beta blockers will not experience the neurogenic (SNS) symptoms before developing neuroglycopenic (cellular) symptoms

68
Q

What is the most common precipitating factor in DKA?

A

Illness

69
Q

Why do type 1 diabetics go into a coma at a lower blood glucose than type 2 diabetics?

A

Diabetics go into a coma due to acidity and osmolarity change. Type 1 diabetics experience both, but type 2 diabetics do not experience as much acidity due to the presence of insulin.

70
Q

Why do some patients in DKA manifest with Kussmaul breathing?

A

They express Kussmaul breathing in an attempt to breathe off CO2, which has been increasing due to the metabolic acidosis

71
Q

Why is IV insulin preferred over SQ in the treatment of DKA?

A

Patients in DKA are usually dehydrated, which reduces the SQ absorption

72
Q

When treating a patient in DKA, why do we supplement with K+ if their serum K+ is normal?

A

We’re also giving them IV insulin, which transports K+ into cells… want to prevent hypokalemia

73
Q

What is the bolus dose of insulin to begin treating DKA?

A

0.1 U/kg IV push

74
Q

With what does CNS depression correlate in HHNKC?

A

Degree of hyperosmolarity

75
Q

How would you advise a type 1 diabetic to avoid the Somogyi effect?

A

Eat a protein-rich snack prior to bedtime to prevent nocturnal hypoglycemia

76
Q

How does the aldose reductase pathway contribute to chronic DM complications?

A

Results in sorbitol production, which binds to basement membranes around vessels and nerves

77
Q

What results from protein kinase C activation, a chronic complication of DM?

A

Large vessels become much less compliant and small vessels have problems with nutrient diffusion due to proliferation of endothelial and smooth muscle cells

78
Q

A patient with type 2 DM wants to know if they can lower their risk for macro- and microvascular complications by lowering their A1C. What should you tell them?

A
  • Improvement in A1C has not led to improved macrovascular outcomes (atherosclerosis)
  • Improvement in A1C has improved microvascular outcomes
79
Q

What are the stages of retinopathy in a patient with DM?

A
  • Non-proliferative
  • Pre-proliferative
  • Proliferative
80
Q

What are some histologic findings you might expect to find in a diabetic patient with nephropathy?

A
  • Hyaline arteriolosclerosis
  • Thickened glomerulus basement membrane
  • Thinning of functional cortical tissue
  • Diffuse and nodular glomerulosclerosis
81
Q

Are sensory or motor nerves affected first by diabetic neuropathy?

A

Sensory

82
Q

Are myelinated or unmyelinated neurons affected first by diabetic neuropathy?

A

Unmyelinated

83
Q

What are the 3 classes of hormones?

A
  • Peptide and protein
  • Steroid
  • Amine
84
Q

What are the 2nd messenger systems for protein hormones?

A
  • Adenylate cyclase
  • Phospholipid
  • Guanylate cyclase
  • Tyrosine kinase
85
Q

How would a patient’s levels of free hormones be affected by low serum proteins?

A

The patient would have more free (active) circulating hormone since less hormone would be bound

86
Q

Why does it take so long for thyroid hormones to reach therapeutic levels?

A

Thyroid hormones are highly protein-bound

87
Q

What types of hormones are metabolically cleared quickly?

A

H2O-soluble hormones like insulin, ADH, testosterone, and aldosterone

88
Q

Which pituitary hormones would be affected by a clot in the portal system?

A
  • TSH
  • Prolactin
  • FSH/LG
  • ACTH
  • MSH
  • Growth hormone
89
Q

What is the most prevalent cell type in the anterior pituitary?

A

Somatotrophs

90
Q

What symptoms would you expect in a patient experiencing mass effects from a pituitary adenoma?

A
  • Bitemporal hemianopsia
  • Increased ICP
  • Pituitary apoplexy
91
Q

Would you expect to find a larger tumor with a functioning or non-functioning pituitary tumor? Why?

A

Non-functioning, you would see symptoms early in a functioning tumor but a non-functioning tumor can get big before you see mass effect symptoms

92
Q

Most pituitary adenomas are _________ in origin.

A

Monoclonal

93
Q

What are some causes of hyperprolactinemia that must be ruled out before considering a tumor?

A
  • Interruption of dopamine due to head injury
  • Psychotropic drugs
94
Q

What is the worst hormone to live without?

A

Cortisol, won’t live >6 weeks without it

95
Q

What are the results of a ACTH/cortisol deficiency?

A
  • Loss of functional maintenance of cells
  • Hypoglycemia
  • Limited maximum aldosterone secretion
96
Q

What is the most common cause of Cushing’s syndrome?

A

Cushing’s disease

97
Q

What long-term effects can untreated Cushing’s syndrome cause?

A
  • Infertility
  • Hypothyroidism
  • Shorter stature than expected
98
Q

What must be demonstrated to diagnose pituitary carcinomas?

A

Metastatic disease

99
Q

What is the most common cause of SIADH?

A

Ectopic production

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