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From Flashcardlet > Patho SS Exam 2 > Flashcards

Patho SS Exam 2 Flashcards

1
Q

Paralysis Agitans

A

Another name for Parkinson’s disease, was initially termed this in 1817

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2
Q

Lewy Body Disease

A

Inclusion bodies accumulate in the substantia nigra and interfere with cell function.

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3
Q

What kind of neurons are in the Substantia Nigra?

A

Dopaminergic Neurons

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4
Q

Secondary Parkinsonism

A

Caused by things like mediations (antiphsychotocis), Illicit drugs (MPTP), Multi infarctions in the substantia nigra and post encephalitis.

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5
Q

What is MPTP

A

a drug that is taken IV and is rapidly consumed by the Substantia Nigra, destroying it and cuasing catatonia within weeks.

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6
Q

What neurotransmitter does the nigral striatal pathway release? How is it impacted by Parkinson’s?

A

It releases dopamine onto the C & P straitum. The dopamine release is decreased in Parkinson’s.

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7
Q

What kind of neuron is in the C & P Striatum that receives Dopamine from the nigral striatal pathyway, and how is it impacted by Parkinson’s?

A

An anticholinergic neuron that is normally inhibited by dopamine, when dopamine is decreased in Parkinson’s then it releases more Ach onto the next neuron.

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8
Q

What kind of neuron receives Ach in the C & P striatum? How is it impacted by Parkinson’s?

A

It is a GABA neuron. The increased Ach stimulates excess GABA release from this neuron.

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9
Q

What kind of neuron receives GABA in the Globus Palidus Externa? How is it impacted by Parkinson’s?

A

It is a GABA neuron and it is inhibited by the GABA it receives from the C&P Striatum. This decreases the amount of GABA it releases on the next neuron.

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10
Q

What kind of neuron is in the Subthalamic nuclei? How is it impacted by Parkinson’s?

A

It is a Glutamate neuron that is normally inhibited by GABA. When GABA is decreased there is more glutamate released.

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11
Q

What kind of neuron is in the Globus Pallidus Interna? How is it impacted by Parkinson’s?

A

It is a GABA neuron that is stimulated by glutamate. Since glutamate is increased in parkinson’s, it increases GABA release.

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12
Q

What kind of neuron is in the Thalamus? How is it impacted by Parkinson’s?

A

It is a glutamate neuron that is inhibited by GABA. Since GABA release is increased, there is a decreased amount of glutamate released to the cortex causing poverty of movement.

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13
Q

What is the disease that is caused by an excess of dopamine and has an opposite effect on the pathway of Parkinson’s?

A

Huntington’s Disease.

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14
Q

What effect does the cortex have on the dopamine pathway of Parkinson’s?

A

In a cortex without Parkinson’s there is glutamate released onto the C & P Striatum to decrease the activity of the Ach neuron.

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15
Q

What is destroyed in a Pallidotomy and why?

A

The globus pallidus externa so that it does not inhibit the thalamus’ release of glutamate to the cortex.

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16
Q

What is seen on neuropathology of the brain of a patient with Parkinson’s?

A

Depigmentation of the substantia nigra, neuronal loss of the substantia nigra and Lewy bodies on autopsy.

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17
Q

Festinant gait

A

hurried steps to avoid overbalancing (leaning forward and they look like they will fall)

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18
Q

cogwheel

A

resistance to passive movement that will allow for sudden movement and the stop again. Seen in Parkinson’s disease.

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19
Q

What are the cardinal manifestations of Parkinson’s?

A 
TRAPS
Tremor
Ridgity
Akinesia
Postural instability
Soft and monotone speech
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20
Q

Blepharoclonus

A

when the eyelids are pushed down they flutter with clonus.

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21
Q

What are the autonomic manifestations of Parkinson’s?

A

Orthostatic hypotension, urine retention, seborrhea, depression, anxiety and dementia.

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22
Q

What are the cardinal physical manifestations on PE for Parkinson’s?

A

Lack of convergence, exaggerated glabellar tap, blepharoclonus, head drop/head rigidity.

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23
Q

What is stage I Parkinson’s disease?

A

Unilateral involvement with mild functional impariment.

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24
Q

What is stage II Parkinson’s disease?

A

Bilateral involvement but balance is okay.

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25
Q

What is stage III Parkinson’s disease?

A

Postural unsteadiness but is not incapacitating

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26
Q

What is stage IV Parkinson’s disease?

A

Movement disabling with rigid bradykinesia.

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27
Q

What is stage V Parkinson’s disease?

A

Confined to bed with cachexia, wheelchair and constant care.

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28
Q

How do you rule out Wilson’s disease?

A

Look for Kayser-Fleisher rings (copper deposits on the iris and in the substantia nigra).

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29
Q

What is Selegiline (Eldepryl)?

A

An MAO-B inhibitor used in the medical treatment of Parkinson’s disease. This increases dopamine by blocking MAO breakdown of it.

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30
Q

What is Tasmar (Tolcapine)?

A

A COMT inhibitor used in the medical treatment of Parkinson’s disease. This increases dopamine by blocking COMT breakdown of it. CAUTION it’s hepatotoxic.

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31
Q

What are Cogentin (Benzotropine) and Artane?

A

Anticholinergic medications that block the increased Ach activity in the C&P Striatum to prevent the increased GABA in the subsequent pathway.

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32
Q

What are Parlodel (Bromocriptine) and Permax (Pergolide)?

A

Dopamine agonists used in the medical treatment of Parkinson’s. Side effects are prevention of prolactin release, psychosis, hallucinations and (Valvular disease with Permax).

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33
Q

What is Amantadine?

A

A dopamine reuptake inhibitor that allows dopamine to remain in the synpatic cleft to block Ach release in the striatum.

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34
Q

What are L-dopa and Carbidopa?

A

Sinemet. Prevent the carboxylation of L-dopa in the blood stream so that it can get into the blood since L-dopa can cross the blood brain barrier. Side effects are dyskinesia, nausea and vomiting.

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35
Q

What is the on-off phenomena seen with Sinemets?

A

protein competes for absorption causeing this variability between immobility and incapacity followed by periods of free movement.

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36
Q

What is the wearing off phenomena seen with Sinemets?

A

re-emergence of manifestations at the end of the drugs life in the body when less L-Dopa is reaching the brain.

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37
Q

What should be used/avoided in adults >60 with Parkinson’s?

A

Use: Sinemet and add a dopamine agonist.
Avoid: Selegiline, amantadine, and anticholinergics

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38
Q

What should be used in adults 50-59 with Parkinson’s?

A

Use: Selegiline and Dopamine Agonist.
Add: Sinemet, amantadine

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39
Q

What should be used in adults <50?

A

Use: selegeline, amantadine and anticholinergics

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40
Q

What are the surgical treatments for Parkinson’s?

A

Pallidotomy - impacts the GP-E but may recur within 6 months
Thalmotoy - ventral, only unilateral or bilateral which can cause dysarthria.
Thalamic and Subthalamic stimulation bilaterally. This is reversible.

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41
Q

How is the Globus pallidus reached? What are the approach concerns?

A

Reached through the internal capsule and if the probe is too far down there will be optic tract disturbance and visual loss, is too far medially there will be contralateral motor loss.

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42
Q

What are some of the risk factors of schizophrenia besides genetics?

A

Living in an urban area, immigration, obstetrical complications, late winter-early spring time of birth and advanced paternal age at the time of conception.

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43
Q

What are the common co-occurring conditions with schizophrenia?

A

Depression, anxiety and alcohol/substance abuse and dependency.

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44
Q

What are the 4 As of negative symptoms for schizophrenia?

A

Affective disorder - inappropriate affect, poor eye contact, unchanging facial expressions.
Alogia - poverty of speech, thought blocking, latency of response.
Apathy - poor grooming and hygiene, anergy
Asocialty/anhedonia - failure to engage with peers, little interest in sex/intimacy.

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45
Q

What are the cognitive manifestations of Schizophrenia?

A

deficits in processing, verbal learning and memory and verbal comprehenison.

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46
Q

What are the physical manifestations of Schizophrenia?

A

Neurological disturbances - agraphesthesia and asterogenesis, poor motor coordination and sequencing because of DA blocking in the extrapyramidal system and left-right confusion.
Catatonia
Metabolic disturbances - diabetes, hyperlipidemia, and hypertension.

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47
Q

what types of sx do 1st generation antipsychotics work best for?

A

positive

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48
Q

what types of sx do 2nd generation antipsychotics work best for?

A

mixed positive and negative

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49
Q

what are the neuroanatomic alterations schizophrenia?

A

enlargement of the lateral and third ventricles, widening of the frontal cortical fissures and sulci. Loss of cortical neurons.

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50
Q

What are the neurotransmitter alterations in schizophrenia?

A

Excess dopamine, excess serotonin and decreased/altered glutamate activity.

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51
Q

What are the side effects of typical antipsychotics (Haldol, Thorazine)?

A

sedation, hyperprolactinemia, bradykinesia, maskline facies, prolonged QT interval and tardive dyskinesia

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52
Q

What are the side effects of atypical antipsychotics (Zyprexa, Risperidol, Geodon)

A

decreased risk of Tardive dyskinesia, but risk of metabolic syndrome, weight gain, agranulocytosis.

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53
Q

What do you do at the first sign of tardive dyskinesia and why?

A

Wean off the medication because once it starts it’s hard to get rid of. Get them off the med before it’s severe.

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54
Q

What is the dopamine hypothesis and what dopamine receptor is believed to be involved in Schizophrenia?

A

There are 5 types of dopamine receptors that are believed to be involved in various disorders. D2 inhibits adenylyl cyclase and is associated with schizoprenia, recurrent depression, adolescent emotional disorders, alcholism and parkinson-like disorders.
When DA is overactive in the mesolimbic pathway it causes positive sx.
When DA is overactive in the mesocortical pathway it causes positive and negative sx.

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55
Q

What is the serotonin hypothesis?

A

Serotonin receptors are involved in the psychotomimetic and psychogenitc properties of hallucinations, and there is an altered number of cortical 5-HT receptors in schizophrenic brains, and the polymorphisms of the 5-HT receptor genes are associated with schizophrenia.

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56
Q

What is the glutamatergic hypothesis?

A

things like phencyclidine and ketamine are both non-competitive antagonists of NMDA subtype glutamate receptor and they induce schizophrenia-like symptoms and worsen some of the sx of schizophrenia, and decreased NDMA is a predisposing factor for schizophrenia. It’s believed that glutamate must play a role in schizophrenia, it works as a brake to DA release, so when it’s absent or not functioning properly then it allows for increased DA release.

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57
Q

What is the difference between mood and affect?

A

Mood is a sustained emotional state

Affect is a brief emotional feeling.

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58
Q

What are the neuroendocrine dysregulations associated with depression?

A

Hypothalamic-Pituitary-Adrenal System dysregulation causing an altered cortisol production pattern.
Hyopthalamic-Pituitary-Thyroid system dysregulation.
Increased CSF levels of TRH, blunted TSH response to TRH challenge, decreased nocturnal rise in TSH - therefore, draw a TSH level before final diagnosis.

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59
Q

What does dexamethasone do in relation to depression?

A

results in an increase in cortisol instead of a decrease because of HPT alteration.

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60
Q

What are the effects of HPT dysregulation in mood disorders?

A

Altered HPT system - dexamethasone causes in increase in cortisol rather than a decrease.
Increase CSF levels of TRH
Blunted TSH in response to TRH challenge
Decreased nocturnal rise in TSH.

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61
Q

What is the difference between the exocrine pancreas and the endocrine pancreas?

A

The exocrine pancreas secretes into the ductal system to the duodenum while the endocrine pancrease secretes into the bloodstream.

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62
Q

What types of cells secrete exocrine pancrease enzymes? What are the exocrine pancreatic enzymes and their function?

A 
Acini cells
Amylase - carb breakdown
Lipase - fat breakdown
DNA-ase - nucleic acid breakdown
RNA-ase - nucleic acid breakdown
Zymogens:  Trypsinogen Chymotrypsinogen, procarboxypeptidase A, B
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63
Q

What types of cells secrete endocrine products? What are the endocrine products produced by each type of cell?

A 
Islets of Langerhans 
Beta cells (60% of islets) release insulin
Alpha cells (25% of islets) release glucagon
Delta cells (10% of islets) release somatostatin
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64
Q

What enzyme degrades insulin when it is released?

A

insulinase

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65
Q

how is insulin packaged?

A

Insulin (alpha and beta chains) and C peptide are packaged in secretory granules and released together. Only 5-10% is secreted in the form of proinsulin

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66
Q

what is proinsulin?

A

The storage, non-functional form of insulin that is connected - contains the alpha, beta and C-peptide chains.

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67
Q

How is C-peptide important in measuring insulin release?

A

Insulin has a very short life in the serum, it is taken up by cells quickly. C-peptide remains in the serum for longer, so if a patient has no c-peptide in their serum then you know that they don’t release insulin, but if they have c-peptide in the serum then they do release insulin (can distinguish TI from TII)

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68
Q

What are the functions of insulin?

A

Insulin binds to its receptor and causes the activation tyrosine kinases and phosphorylation of enzymes. These enzymes cause glucose synthesis in the liver, synthesis of fat and synthesis of proteins (prevents the breakdown of these things) as well as growth and gene expression and the phosphorylation of the glucose transporter that is inserted into the cell membrane to allow for glucose to enter the cell.

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69
Q

What is the name of the transporter that is inserted into the membrane of the cell when stimulated by insulin?

A

GLUT-4

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70
Q

What is the mechanism of glucose-stimulated insulin secretion?

A

Glucose enters the beta cell through the GLUT-2 receptor, is processed in the mitochondria to make ATP to cause the K+ channel in the membrane to be deactivated. This depolarizes the membrane causing Ca++ to move into the cell and push insulin out of the cell.

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71
Q

What does it mean for a transporter to be insulin independent?

A

The transporter is always in the cell membrane, with or without the presence of insulin. GLUT1 and GLUT-2 are examples.

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72
Q

Where is GLUT-1 located?

A

in the GI tract and the distal segment of the renal tubules

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73
Q

Where is GLUT-2 located?

A

in the beta cells and proximal segment of the renal tubules.

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74
Q

What are the side effects of a non-specific GLUT receptor blocker for the treatment of diabetes?

A

They cause severe diarrhea because they block the GLUT-1 in the GI tract.

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75
Q

What are the side effects of a specific GLUT-2 receptor blocker for the treatment of diabetes?

A

It blocks the renal reabsorption of glucose, causing the patient to pee out excess glucose. This is contraindicated in patients with renal failure. These may decrease blood pressure, cause weight loss and increase LDL 1-2%.

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76
Q

What is the mechanism of the sulfonylureas?

A

They block the K+ channels in the beta cell causing it to be depolarized and releasing insulin.

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77
Q

What does insulin do in the muscles?

A

It increases glucose and amino acid uptake.
Stimulates storage: glycogenesis, lipogenesis, and protein synthesis.
Inhibits breakdown: gluconeogenesis, glycogenolysis, ketogenesis (lipolysis), and proteolysis.

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78
Q

What does insulin do in the liver?

A

Increase glucose uptake.
Stimulates storage: glycogenesis, lipogenesis, and protein synthesis.
Inhibits breakdown: Gluconeogenesis, glycogenolysis, and ketogenesis (lipolysis) ~ note that it does not impact proteolysis in the liver!

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79
Q

What does insulin do in the adipose tissue?

A

Increase glucose uptake.
Stimulate storage: lipogenesis
Inhibit breakdown: ketogenesis(lipolysis)

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80
Q

How does fat increase the risk of T2 diabetes?

A

There is fat stored in and out of the cell. More fat inside the cell causes the production of substances that make insulin resistant within the cell, so phosphorylation does not occur when glucose binds to the cell and the transporter is not inserted into the membrane.

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81
Q

What factors influence the secretion of insulin?

A

Stimulated by: glucose, amino acids, free fatty acids, and some by GI hormones and neural influence by PNS and SNS activation.
Inhibited by: SNS activity, fasting and exercise.

82
Q

How do beta adrenergic cells influence insulin secretion?

A

beta adrenergic cells have both alpha and beta receptors, if the beta receptors are activated then it increases release and if alpha receptors are activated then it decreases release. Some HTN drugs work on these receptors so they can change the blood glucose - that’s why ACE-I is preferred for a diabetic over a beta blocker.

83
Q

What are the effects of glucagon?

A

to increase plasma glucose, free fatty acids, ketoacids and decrease plasma amino acids.

84
Q

What factors influence the secretion of glucagon?

A

Stimulated by: hypoglycemia, amino acids, CKK and Gastrin, Fasting and Exercise and Neural influences such as beta adrenergic stimulation and vagal activity.
Inhibited by: Glucose, insulin (direct effect), Secretin, GLP-1, FFAs, ketoacids and neural influences like alpha adrenergic stimulation.

85
Q

How does the fight-flight response impact blood sugar?

A

Increased SNS activity causes insulin and glucagon release so that the blood sugar is decreased by the insulin but increased by glucagon to maintain a balance during crisis response.

86
Q

How do amino acids impact blood sugar?

A

amino acids increase insulin and glucagon secretion. This causes stimulation of storage and decreased blood sugar by the insulin and breakdown of proteins and glycogen to increase the blood sugar by glucagon. This acts to balance the effects.

87
Q

What is the diagnostic criteria for DM?

A

FBG >/= 126mg/dl
OGTT >/=200 mg/dl @ 2 hours
A1C >/= 6.5%

88
Q

What is the diagnostic criteria for impaired glucose tolerance?

A

FBG 110-125mg/dl
OGTT 140-199mg/dl @ 2 hours
A1C 5.7-6.4%

89
Q

What are normal values for blood sugar labs?

A

FBG <5.7%

90
Q

What is the A1C goal for patients with DM?

A

<7%

91
Q

What is MODY?

A

Maturity Onset Diabetes of the Young. There are mutations in a variety of genes causing primary beta cell defects and glucokinase mutations. This causes T2 diabetes to occur in a young patient, not due to obesity in adolescence.

92
Q

How is the human placental lactogen involved in gestational diabetes?

A

It is produced by the placenta and gets into the mother causing insulin resistance, so blood glucose increases.

93
Q

What type of monitoring should be done post delivery on a female who had gestational diabetes?

A

They should have glucose monitored because 1/3 will return to normal, 1/3 will return to normal but be predisposed to developing diabetes and 1/3 will have overt diabetes.

94
Q

What is metabolic syndrome?

A 
Abdominal obesity
insulin resistance
fasting hyperglycemia
increased lipids 
hypertension
95
Q

Why does polyuria occur in diabetic patients?

A

Once the renal threshold is met for blood glucose, the excess begins to spill in the urine. Typical renal threshold is 180.

96
Q

Why does polydipsia occur in diabetic patients?

A

Increased thirst to replace the fluid lost due to polyuria (water is pulled osmotically into the urine with glucose). The plasma osmolality increases, therefore triggering the thirst center in the hypothalamus.

97
Q

Why does polyphagia occur in diabetic patients?

A

The cells are not getting the glucose that’s in the blood so the body thinks it’s starving and increases hunger.

98
Q

What are the characteristics of T1 diabetes?

A

autoimmune destruction of the beta cells causes complete lack of insulin. Genetic mutations (HLA-DR4 and HLA-DR3) are present. 85-90% have an islet cell autoantibody.

99
Q

What is the initial presentation of T1 diabetes?

A

polyuria, polydipsia and polyphagia with a sudden onset, may be in DKA when they arrive for initial assessment.

100
Q

What are the characteristics of T2 diabetes?

A

generally an adult onset related to genetic predisposition and lifestyle. The cells in the body become resistant to insulin, causing the body to improperly use insulin.

101
Q

What is the initial presentation of T2 diabetes?

A

may be asymptomatic because the symptoms are so gradual in onset. May have complications of hyperglycemia such as Pruritis, fatigue, recurrent infections, visual changes and paesthesias.

102
Q

What causes infection in diabetic patients?

A

decreased sensation, tissue hypoxia, pathogens that proliferate well in the presence of excess glucose, decreased delivery of WBCs and decreased/altered WBC function.

103
Q

What are the three types of islet cell tumors? Are they rare or not?

A

Insulinomas (NOT rare) of the beta cells
Glucagonomas (rare) of the alpha cells
Somatostatinomas (rare) of the delta cells

104
Q

What produces Zollinger-Ellison Syndrome?

A

Gastrinomas, consisting of increased acid and ulcers.

105
Q

What is considered hypoglycemia in a newborn? Children or adults?

A

<45-60 in a child or adult

106
Q

what causes hypoglycemia?

A

too much insulin, decreased calorie intake, exercise, too much medication.

107
Q

What effect to beta blockers have on hypoglycemia?

A

They make it so the patient won’t feel the symptoms of hypoglycemia, so you have to educate them about it and make sure they know how to address it.

108
Q

What is the treatment for hypoglycemia?

A

supplement glucose: tablets, gummies, juice.

continue working with a nutritionist to find what works best for them.

109
Q

What are the symptoms of hypoglycemia?

A

Nervous system: Tachycardia, diaphoresis, tremors, pallor and anxiety.
Cellular: Headache, dizzy, irritable, fatigue, confusion, vision changes, hunger, seizure and coma.

110
Q

What is the most common precipitating factor of DKA?

A

illness

Stress response -> Insulin resistance -> increased plasma glucose -> release of cortisol, epi, GH -> mobilization of stored nutrients -> increased plasma glucose but cells don’t get it causing further release of cortisol, epi and GH.

In initial presentation of T1, take out the first two steps and sub for lack of insulin

111
Q

What type of diabetic gets DKA?

A

Generally type 1 because they don’t have any insulin around to prevent the break down of FFA to ketones.

112
Q

What are the manifestations of DKA?

A

Classic manifestations, dehydration, kussmaul breathing to blow off acid as CO2, CNS depression, anorexia, nausea and vomiting (caused by CNS when glucose increases by too much).

113
Q

What is the process of DKA?

A

Lack of insulin - hyperglycemia - increased release of glucagon, epi, cortisol and GH - increased lipolysis - increase in FFA in the blood (beta hydroxybutyric acid) - ketone body formation - metabolic acidosis
also in response to ketone bodies - polyuria - volume depletion - dehydration - increased plasma osmolality - CNS Depression and polydipsia.

114
Q

How high is the glucose in a patient with DKA that could put them into a coma?

A

350mg/dl

CNS depression is due to decreased pH and hyperosmolarity.

115
Q

How high is the glucose in a patient with HHS that could put them into a coma?

A

600-800mg/dl

CNS depression is due to the hyperosmolarity.

116
Q

How do you treat DKA?

A 
IV fluids (1 L in first 30 mins, 2nd L in next hr, 3rd L in next 2 hrs, 4th L in next 4 hrs)
IV K+ if serum K+ is <5.3
117
Q

What kind of IV fluid do you give a diabetic patient in DKA?

A

Normal saline until you know their electrolyte state because you don’t want to cause diabetic encephalopathy.
You can switch them to a different kind of saline when the Na+ is corrected and it won’t cause cells to swell.

118
Q

What is HHNKC

A

more common in T2 diabetics. Extremely high glucose levels and severe volume loss and dehydration that occurs over time. There is insulin present, so it prevents the breakdown of TAGs, so the patient does not become acidotic and there are no ketones. Treat just like DKA.

119
Q

When can IV insulin be stopped in the treatment of DKA and HHNKC?

A

When the blood glucose is <200 for DKA and <300 for HHS, and they can tolerate PO. If they can’t tolerate PO, then keep them on the IV but also give IV dextrose to prevent hypoglycemia.

120
Q

What are the manifestations of HHNKC?

A

glycosuria, polyuria, extreme hyperglycemia, increased serum osmolarity leading to severe dehydration, CNS depression is correlated to the level of serum hyperosmolarity.

121
Q

What is the Somogyi effect?

A

nocturnal hypoglycema because of increased insulin sensitivity followed by rebound hyperglycemia. Manifests with nightmares and morning headaches. Treated with a protein rich snack prior to bed because it stimulates the release of glucagon to prevent the hypoglycemia.

122
Q

What is the dawn effect?

A

Cortisol and GH are increased at night mobilizing the breakdown of substrates, causing morning hyperglycemia - but it’s not rebound because there’s no initial hypoglycemia.

123
Q

Where does microvascular disease present in a diabetic patient?

A

In the kidneys, retina and nerves are the most impacted.

124
Q

How does macrovascular disease present in a diabetic patient?

A

Atherosclerosis in the medium and large arteries that can lead to CAD and CVA.

125
Q

How does protein glycation impact the diabetic patient?

A

The covalent bonds in glycosylation contributes to the thickening of the basement membrane in the vasculature.

126
Q

How does the aldose reductase pathyway impact the nerves in a diabetic patient?

A

within a neuron glucose is converted to sorbitol quickly which is then slowly converted to fructose. Sorbitol can stay in the cell or release and thicken the area around the cell slowing its action potentials.

127
Q

How does Protein Kinase C activation impact the vessels?

A

It increases micro vascular contractility and permeability while proliferating the endothelial and smooth muscle cells - this increases thickness, decreases compliance and decreases diffusion of nutrients.

128
Q

How does diabetes increase the risk of atherosclerosis?

A

Glucose deposits in the arteries making it easier for lipids to deposit.

129
Q

What are the manifestations of retinopathy?

A

Microaneurysms, hemorrhages, cotton wool spots, hard exudates, venous beading, neovascularization, retinal detachment, vitreous detachment, pre-retinal hemorrhage

130
Q

What is stage I retinopathy?

A

non proliferative.

Increased retinal capillary permeability, vein dilation, microaneurysm formation and superficial and deep hemorrhages.

131
Q

What is stage II retinopathy?

A

preproliferative.

Progressive retinal ischemia with areas of poor perfusion resulting in infarctions.

132
Q

What is stage III retinopathy?

A

proliferative.
Presence of neovascularization and fibrous tissue formation within the retinal or optic disc. May see retinal detachment or hemorrhage into the vitreous humor.

133
Q

What will happen if exudates, edema or ischemia occurs near the fovea?

A

serious visual loss.

134
Q

What are the results of nephropathy from diabetes?

A

hyaline deposition, thickened basement membranes, gaps between the podocytes allow proteins to leak through.

135
Q

What is the gross appearance of the kidneys that have nephropathy?

A

Diffuse granular surface with marked thinning of the cortical tissue - the functional cortex thins but the rest of the cortex thickens with fibrosis.

136
Q

What are Kimmelsteil-Wilson Kidneys?

A

Nodular glomerulosclerosis of the kidneys that is characteristic of diabetes.

137
Q

What are the causes of neuropathy in diabetes?

A

Metabolic - the neurons have excess sorbitol deposited around the cell body interefering with the diffusion of substances and therefore interfering with function.
Vascular - peripheral vascular disease decreases blood flow to the nerves causing nerve cell death.

138
Q

What are the 2 stages of neuropathy?

A

Subclinical - slowed motor and sensory nerve conduction without manifestations (only detected by good PE!)
Clinical - symptoms are present. Sensory is lost before motor, and moves distal to proximal. Unmyelinated neurons are impacted first.

139
Q

How does SNS and PNS neuropathy present?

A

Gastroparesis and postural hypotension are common presentations.

140
Q

What are the common infections of diabetes?

A

Skin carbuncles and cysts d/t decreased sensation.
Lungs - PNA, TB, URI d/t tissue hypoxia allowing for anaerobe growth.
Kidneys - pyelonephritis because the pathogens proliferate well in urine with high glucose content.
Multiple locations for Candida.

Decreased delivery and function of WBCs make it difficult to fight infection.

141
Q

What are the classes of hormones?

A

Peptide and Protein Hormones, Amine Hormones - Water soluble so they have their receptors on the cell surface and a secondary messenger system works to activate the cell’s hormone pathway.

Steroid hormones - fat soluble so they have their receptors within the cells rather than on the cell surface.

142
Q

What are the mechanisms of action of protein hormones?

A

Secondary messenger systems: Adenylate Cyclase, Phospholipids, Guanylate Cyclase, and Tyrosine Kinase

143
Q

What is the mechanism of action of steroid hormones?

A

direct intracellular action on the adrenal cortex, testes, ovaries, copus luteum, placenta and kidney.

144
Q

what is 1,25-dihydrosycholecalciferol?

A

Activated Vitamin D produced by the kidney.

145
Q

What is the pathway for the synthesis of amine hormones?

A

Tyrosine to L-Dopa, to Dopamine (in dopaminergic neurons), to Norepinephrine (in adrenergic neurons), to Epinephrine ( in the adrenal glands)
OR
Tyrosine to Thyroid Hormone (in the thyroid)

146
Q

What amine hormone is made by the hypothalamus?

A

Dopamine

147
Q

What amine hormones are made by the Thyroid?

A

T3 and T4

148
Q

What amine hormones are made by the adrenal medulla?

A

NE and Epi

149
Q

Once a hormone is released from the endocrine cell, what can happen to it?

A

It can go one of 3 ways:

  1. Bind to protein and be inactive
  2. Be degraded
  3. Bind to receptor and have a biological effect
150
Q

What happens to free hormone levels if protein levels are increased, or decreased

A

Increased - less free hormone

Decreased - more free hormone

151
Q

What hormones are highly protein bound?

A

T3 and T4, Cortisol and Testosterone

152
Q

What hormones are not highly protein bound?

A

Aldosterone, TSH, Insulin, ADH

153
Q

What hormones are released by the hypothalamus, and what is their impact on the anterior pituitary?

A

Growth hormone releasing hormone (GHRH -> GH release), Somatostatin (GIH -> decrease GH release), Corticotropin Releasing Hormone (CHR -> ACTH), Thyroid releasing hormone (TRH -> TSH), Gonadotropin releasing hormone (GnRH -> FSH, LH), Prolactin Inhibiting Hormone (PIH -> decreased Prolactin release)

154
Q

How is the anterior vs. posterior pituitary connected to the hypothalamus?

A

Anterior - connected via vascular supply

Posterior - connected by nerve endings

155
Q

What is released by the posterior pituitary?

A

ADH is made by the Supraoptic nuclei and Oxytocin is made by the Paraventricular nuclei in the hypothalamus and released from the neurohypophysis.

156
Q

What happens if there is a clot in the blood supply to the anterior pituitary?

A

panhypopit occurs.

157
Q

What is hyperpituitarism?

A

a functional benign tumor, hyperplasia or carcinoma causes increased release of one hormone and therefore decreased release of other hormones due to mass effect.

158
Q

If a patient has a prolactinoma, what happens to their hormones?

A

They have increased prolactin release, decreased GH, ACTH, TSH, FSH and LH release.

159
Q

What are the local mass effects of an anterior pituitary adenoma

A

bitemoporal hemianopsia, ICP, hemorrhage into an adenoma resulting in rapid enlargement of lesion-pituitary apoplexy.

160
Q

What effects do you see first if you have a non-secreting pituitary tumor?

A

You will see the mass effects first because the secretory effects will be decreased.

161
Q

What percent of intracranial tumors are pituitary adenomas?

A

~10%

162
Q

What percent of routine autopsies reveal pituitary incidentalomas?

A

~25%

163
Q

What is the difference between a micro and macro adenoma?

A

micro 1cm

164
Q

What are the genetic abnormalities associated with pituitary adenomas?

A

Mutations in the G-protein system (GNAS gene codes for the alpha subunit which is a common mutation)
Mutations in the tumor suppressor gene
~5% have an inherited predisposition.

165
Q

What is the most common functional pituitary tumor?

A

prolactinoma - ~ 30%
prolactin release is proportional to pituitary size, and may undergo dystrophic calcification and produce a pituitary stone.

166
Q

What inhibits prolactin production?

A

Dopamine release from the hypothalamus. Can be inhibited also by interruption of dopamine due to a head injury or psychotropic drugs that interfere with dopamine.

167
Q

What are the symptoms of a hyperprolactinemia?

A

Hormone effects: amenorrhea, galactorrhea, loss of libido, infertility.
Mass effects: headache, fatigue, neck pain, seizures, visual field effects.

168
Q

What is the treatment for prolactinomas?

A

Bromocriptine (a dopamine agonist that binds to lactotroph to decrease prolactin release.
Surgery - trans-sphenoid removal of the tumor
radiation

169
Q

What is the second most common pituitary adenoma?

A

Somatotroph adenomas

Hypersecretion of GH stimulates hepatic secretion of IGF-1 which causes the clinical manifestations.

170
Q

What is it called if the somatotroph adenoma occurs in childhood?

A

Gigantism - increased body size & longitudinal bone growth if it occurs prior to bone maturity.

171
Q

What is it called if the somatotroph adenoma occurs in adulthood?

A

Acromegaly - enlargement of the head, hands, feet, jaw, tongue and soft tissues, results in T2 diabetes, and CAD.

172
Q

What is proganthism?

A

enlargement of the jaw with acromegaly

173
Q

What is the difference between cushing’s disease and cushing’s syndrome?

A

Cushing’s disease - increased ACTH from pituitary or an exogenous source.
Cushing’s syndrome - increased cortisol production but not caused by a pituitary problem - can be d/t use of steroids.

174
Q

What are the physical manifestations of cushing’s?

A

extremities lose fat and there is proximal muscle wasting, moon facies, central obesity, striae on the abdomen, supraclavicular fat pad, cervical dorsal fat pad, increased risk of T2 diabetes.

175
Q

What percent of adenomas are FSH and LH producing?

A

10-15%. These are found in middle aged men and women when they become symptomatic due to mass effect.

176
Q

what percent of pituitary adenomas are non-functioning?

A

~25% - they either produce no hormone or a non-functioning product. They present due to mass effect.

177
Q

Are pituitary carcinomas common?

A

No, and to be considered a carcinoma, they have to have proven metastatic disease.

178
Q

What is hypopituitarism?

A

A range of dysfunction from the absence of selective pituitary hormones to the absence of all hormones (panhypopit).

179
Q

What type of hypopit is almost always hypothalamic in origin?

A

hypopit with posterior pituitary dysfunction (i.e. diabetes insipidus).

180
Q

What are the common causes of hypopit?

A

infarction, tumors, head trauma that severs the stalk, vascular malformation in the portal system, infections, rathke cleft cyst in the area where the pituitary sits in the sella tursica, ischemic necrosis (Sheehan syndrome following pregnancy), and empty sella syndrome.

181
Q

What is Sheehan Syndrome?

A

blood supply during pregnancy increases, so the vessels are ingorged. If hemorrhage occurs during labor there is massive bleeding, the vessels will vasospasm as a result and causes ischemia and necrosis of the pituitary.

182
Q

What is a primary cause of empty sella syndrome?

A

a defect in the diaphragma sellae or increased ICP allowing encroachment of arachnoid and CSF into the sella and compressing the pituitary gland.

183
Q

What is a secondary cause of empty sella syndrome?

A

The intervention for a pituitary process (i.e. ademona) which results in the destruction/removal of the pituitary gland.

184
Q

What are the manifestations of ACTH-Cortisol deficiency?

A

hypoglycemia, cortisol is required for normal cell function so this is life threatening, decreased ACTH limits maximum aldosterone secretion which alters the H2O and Na+ balance.

185
Q

What are the manifestations of low FSH/LH?

A

In females: amenorrhea, atrophy of gonadal tissues

In males: atrophy of testes, decreased secondary characteristics.

186
Q

What are the components of the posterior pituitary?

A

modified glial cells, axonal processes extending from the hypothalamus (Supraventricular and paraventricular nuclei).

187
Q

what is oxytocin?

A

a hormone released from the posterior pituitary that is not active until after delivery for milk let down.

188
Q

What is ADH?

A

A hormone released from the posterior pituitary that acts on water conservation by the kidney. ADH release increases when plasma osmolarity increases.

189
Q

What is the presentation of ADH deficiency?

A

Diabetes insipidus - vascular collapse can occur because of extreme diuresis.

190
Q

What is the presentation of ADH excess?

A

SIADH - results in increased H20 reabsorption despite decreased serum osmolarity resulting in hyponatremia. Most tumors that release ADH are from exogenous sources (i.e. small cell lung cancer)

191
Q

What are the causes of SIADH?

A

Ectopic production (i.e. small cell lung cancer)
Pituitary infection
Medications (general anasthetics, narcotics)
Increased ICP

192
Q

What is the result of SIADH?

A

Hypervolumia causes HTN and heart failure.

Hyponatremia/Hyposmolarity based on the dilution of Na+.

193
Q

What symptoms will a patient have if their Na+ is between 130 and 140?

A

anorexia, fatigue, dyspnea

194
Q

what symptoms will a patient have if their Na+ is between 120 and 130?

A

Nausea, vomiting and abdominal cramping

195
Q

What symptoms will a patient have if their Na+ is between 110 and 115?

A

confusion, lethargy, muscle twitching, convulsions

196
Q

overactivity of DA in the mesolimbic pathway produces what type of symptoms in schizophrenia?

A

Positive sx.

197
Q

overactivity of DA in the mesocortical pathway produces what type of symptoms in schizophrenia?

A

Positive and negative sx.

198
Q

How do TCAs work?

A

They block the reuptake of 5-HT > NE > DA, but each one adjusts these three neurotransmitters differently, so you can switch a patient between drugs in this class and may see an improvement.

199
Q

How do SSRIs work?

A

They block the reuptake of 5-HT only. There are fewer side effects with SSRIs than with TCAs.

200
Q

Which location in the brain sends out adrenergic neurons to a variety of places to release NE and have a modulation effect in various parts of the brain?

A

Locus ceruleus.

201
Q

How do MAO-Is work?

A

They block the destruction of neurotransmitters in the synaptic clefts by the enzyme MAO, this allows the neurotransmitter to have a longer time to act in the synaptic cleft.

From Flashcardlet (30 decks)

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