Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Final FA review > 3/8 endo > Flashcards

3/8 endo Flashcards

1
Q

How does excess cortisol lead to HTN?

A
  • up-regulates alpha-1 receptors on arterioles.

- has slight mineralocorticoid ability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Dexamethasone suppression test

  • low dose suppresses ACTH =
  • high dose (8mg) suppresses ACTH =
  • no suppression w/high dose (8mg) =
A
  • low dose suppresses ACTH = normal
  • high dose suppresses ACTH = pituitary adenoma
  • no suppression w/high dose = ectopic ACTH prod.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does excess cortisol lead to osteoporosis?

A

-cortisol dec. osteoblastic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CRH stimulation test

A
  • differentiate btwn a pituitary adenoma and ectopic source.
  • an ectopic source will not increase cortisol production in response to CRH b/c the pituitary is super suppressed by all the negative feedback of the ectopic ACTH.
  • the pituitary adenoma will make even more ACTH and thus cortisol in response to CRH b/c its negative feedback mechanism is obviously fucked up which is a key property thats allowing it to pump out all of this ACTH in the first place.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Inoperable Cushings

-Tx:

A

Ketoconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Primary or secondary hyperaldo

-Tx:

A

-surgery (primary) or spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which bug has been known to destroy the adrenals?

A

TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Waterhouse-Friderichsen syndrome

-potential causes?

A

-Neisseria meningitidis septicemia, DIC, and endotoxic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Resting tone on vasculature?

A
  • sympathetic

- hence neurogenic shock - you lose that sympathetic tone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Neuroblastoma

  • originates from what tissue?
  • presentation?
A
  • Neural crest cells
  • abdominal distension and a firm, irregular mass B that can cross the midline (vs. Wilms tumor, which is smooth and unilateral).
  • it does not cause HTN like pheo does.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neuroblastoma

  • what is increased in urine?
  • associated w/which oncogene?
A
  • Homovanillic acid (HVA) = breakdown product of dopamine.

- N-myc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Homovanillic acid (HVA)

  • inc urinary levels in what disease?
  • HVA is breakdown product of what?
A
  • neuroblastoma
  • breakdown product of dopamine.

*dopamine = precursor to catecholamines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neuroblastoma

  • bombesin + or -
  • what do you see on histology?
A
  • bombesin + (tumor marker)

- rosettes & classic small, round, blue/purple nuclei.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pheochromocytoma

  • arise from what cells?
  • what color is it usually?
A

chromaffin cells

  • neural crest cells
  • brown - the adrenal medulla is usually brown.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

pheochromocytoma

-rule of 10s

A 
Rule of 10’s: 
10% malignant 
10% bilateral 
10% extra-adrenal 
10% calcify 
10% kids

*More than 70% of cases of pheochromocytomas
are bilateral when familial.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

pheochromocytoma

-associated w/which diseases?

A

-Associated with von Hippel-Lindau disease, MEN 2A and 2B.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pheochromocytoma

-Tx:

A

Irreversible α-antagonists (phenoxybenzamine) and β-blockers followed by tumor resection.

  • α-blockade must be achieved before giving
  • β-blockers to avoid a hypertensive crisis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hyperthyroidism

  • diarrhea or constipation?
  • inc or dec reflexes?
A
  • diarrhea

- inc. reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

hyperthyroidism

  • whats the skin & hair like?
  • hypo or hypercholesterolemia?
A
  • Warm, moist skin; fine hair

- Hypocholesterolemia (due to inc. LDL receptor expression). *you’re basically burning more fuel.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hyperthyroidism

  • calcium level?
  • blood glucose?
A
  • hypercalcemia (inc. burn resorption).

- hyperglycemia (gluconeo & glycogenolysis going on).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

dyspnea on exertion

-Sx of hypo or hyperthyroidism

A

hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

large fontanels & macroglossia in children.

-hypo or hyperthyroidism?

A

hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Whats the most common cause of myopathy?

A

hypothyroidism

  • myoedema will be present (edema of muscle s/p percussion), inc. creatine kinase, + other hypothyroid Sxs like weight gain, fatigue, etc.
  • will present w/myalgia, proximal muscle weakness, & cramping.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Abs found in hashimotos thyroiditis

A
  • anti-thyroid peroxidase
  • antithyroglobulin antibodies
  • anti-microsome

*they do not cause the disease, they are byproducts of the disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hashimotos

-HLA association?

A

HLA-DR5

*Pernicious anemia also associated w/HLA-DR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hashimotos

-inc risk of what cancer?

A

non-Hodgkin lymphoma
-chronic inflammatory states like hashimotos (or sjogrens or h.pylori gastritis) inc. risk of developing a marginal zone lymphoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hürthle cells

-which disease?

A

hashimotos thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which hypothyroid states can present w/initial transient hyperthyroid state?

A
  • hashimotos

- Subacute thyroiditis (de Quervain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Long standing hashimoto pt that suddenly has an progressively enlarging thyroid, think what?

A

B-cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q 
Congenital hypothyroidism (cretinism)
-Sxs:
A 
The 6 P’s 
Pot-bellied
Pale
Puffy-faced child 
Protruding umbilicus
Protuberant tongue
Poor brain development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Subacute thyroiditis (de Quervain)

  • What type of inflammation?
  • Tx?
A
  • granulomatous inflammation (released colloid acts as a foreign body)
  • aspirin for pain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Reidel thyroiditis

-manifestation of what?

A

-Considered a manifestation of IgG4 -related

systemic disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Wolff-Chaikoff:

A

-Reduction in thyroid hormone levels caused by

ingestion of a large amount of iodine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Histo look of goiter:

A

enlarged follicles and flattened epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Toxic multinodular goiter

A
  • Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor.
  • inc. T4 & T3

*Hot nodules are rarely malignant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Jod-Basedow phenomenon

A

-Thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Thyroid storm

  • most common cause of death?
  • ALP level? why?
A
  • tachyarrythmia

- Inc. ALP due to  bone turnover.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

“scalloping” of the colloid

-which disease?

A

Graves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Are thyroid cancers usually functional?

A
  • no

- and remember, “hot” (functional) nodules are rarely malignant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Thyroid adenomas & carcinomas

-inc or dec iodine uptake?

A

-dec.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

“Orphan Annie” eyes & psammoma bodies

-which disease?

A

papillary carcinoma of thyroid.
-Orphan annie eyes = white clearing in the center of the nucleus

-also see “nuclear grooves” which are dark lines in middle of nucleus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Papillary carcinoma of thyroid

  • inc. risk w/mutations in which genes?
  • inc. risk w/exposure to what?
A
  • RET and BRAF mutations.
  • childhood exposure to radiation.

*-RET - receptor tyrosine kinase encoding gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Orphan Annie eyes

-aka?

A

ground glass nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Follicular carcinoma vs follicular adenoma

A

Follicular carcinoma invades thru the capsule.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Medullary carcinoma

  • which cells?
  • produce what?
  • histo appearance?
A
  • From parafollicular “C cells”; produces calcitonin.

- sheets of cells in an amyloid stroma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Medullary carcinoma

-associated w/which mutations/diseases?

A

-Associated with MEN 2A and 2B (RET mutations).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

osteoclast-like multinucleated giant cells found

-which thyroid cancer?

A

anaplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

hyperparathyroidism

  • urinary cAMP levels?
  • ALP levels?
A
  • high urinary cAMP = PTH works through Gs pathway

- inc ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

hyperparathyroidism & acute pancreatitis

-connection?

A
  • hypercalcemia due to PTH can cause acute pancreatitis.

* high calcium always = chance of metastatic calcification. ie. nephrocalcinosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

hyperparathyroidism

-mnemonic for Sxs

A

“Stones, bones, groans, and psychiatric overtones.”

  • stones = calcium oxalate renal stones
  • bones = osteitis fibrosa cystica
  • groans = constipation
  • depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tertiary hyperparathyroidism

A
  • Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease.
  • very high PTH, high calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Chvostek sign:

  • what is it?
  • sign of what?
A
  • Tapping of facial nerve (tap the Cheek) => contraction of facial muscles.
  • hypocalcemia
53
Q

Pseudohypoparathyroidism (Albright hereditary osteodystrophy):

  • inheritance pattern:
  • what is it?
  • Sxs:
A

-autosomal dominant
-unresponsiveness of kidney to PTH.
-Hypocalcemia, shortened 4th/5th digits, short
stature.

*defective Gs receptors, b/c PTH acts via Gs receptors.

54
Q

Pseudohypoparathyroidism (Albright hereditary osteodystrophy):

  • inheritance pattern:
  • what is it?
  • Sxs:
A

-autosomal dominant
-unresponsiveness of kidney to PTH.
-Hypocalcemia, shortened 4th/5th digits, short
stature.

55
Q

cabergoline

A

dopamine agonist

-like bromocriptine

56
Q

Link btwn GH secreting tumor & DM2

A

GH causes insulin resistance and hyperglycemia.

57
Q

pegvisomant

A

-growth hormone receptor antagonist

58
Q

demeclocycline

A

-ADH antagonist

59
Q

Nephrogenic DI

-Tx:

A

-HCTZ, indomethacin, amiloride, Hydration

60
Q

complete central DI vs partial central DI

A
  • follow water deprivation & subsequent DDAVP admin.

- In pts w/complete central DI, urine osmolarity should rise >50%! So less than 50 would be partial central DI.

61
Q

Does cortisol inc or dec glycogen synthesis in the liver?

A
  • inc. glycogen synthesis!

- seems counter intuitive!

62
Q

Why do glucocorticoids cause muscle weakness?

A

Proteolysis

63
Q

Which organ actually has increased protein synthesis in response to glucocorticoids?

A

Liver
-upregulated proteins (enzymes) involved w/gluconeo & glycogenesis (glycogen synthesis!)

*cortisol increases glycogen synthesis, NOT breakdown!

64
Q

Why does BUN increase w/glucocorticoid administration?

A

Proteolysis!

65
Q

Miglitol

A

alpha glucosidase inhibitors

66
Q

canagliflozin, dapagliflozin

  • mechanism
  • side effects
A

SGLT-2 inhibitors: oral DM drugs.

  • prevent glucose resorption at PCT.
  • causes urinary excretion of glucose.
  • may cause urinary tract & genital mycotic infections due to glucosuria.
  • assess renal fcn before starting this drug.
67
Q

Age range for DM1?

A
68
Q

Fasting blood sugar of _____ of ____ separate occasions is diagnostic of DM.

A

> 126mg/dl, two.

69
Q

PTH level & magnesium

A

-Hypoparathyroidism may be caused by severe hypomagnesemia which can be seen in prolonged diarrhea.

70
Q

Serum chemistry in pseudohypoparathyroidism

  • Ca
  • phosphate
  • PTH
A
  • low Ca
  • high phosphate
  • high PTH
71
Q

Suprasellar mass w/3 components (solid, liquid, calcification) is suggestive of what?

A

craniopharyngioma

72
Q

Renal failure - serum levels of:

  • Ca
  • PTH
A
  • Ca = low

- PTH = high

73
Q

Why is hypernatremia rarely observed in mineralocorticoid excess?

A

Aldosterone escape w/ANP.

  • also, inc. Na and water retention will increase renal blood flow and GFR => inc rate of sodium excretion.
  • ADH also kicks in to keep Na conc. in check.
74
Q

Why do you get profound muscle weakness w/too much Aldo?

-how about parasthesias?

A
  • Hypokalemia leads to muscle weakness.

- hypokalemia & met. alkalosis can cause parasthesias.

75
Q

Stimulation tests are used in times of hormone excess or insufficiency?

A

insufficiency

76
Q

Whats the most common cell type in the ant. pituitary?

A

Somatotrophs

  • make GH
  • 50% of normal pituitary
77
Q

Oxytocin

-made in which nucleus?

A

paraventricular nucleus of hypothalamus

78
Q

SIADH

  • serum Na?
  • volume status?
A

Euvolemic hyponatremia.

  • ADH leads to excess water.
  • Body responds w/dec. aldo.
  • Dec. aldo = losing sodium and water.
79
Q

What happens if you correct SIADH pt’s sodium too quickly?

A

Central pontine myelinolysis

  • neuron dysfunction due to destruction myelin covering neurons in the middle of the brainstem (pons).
  • AKA osmotic demyelination syndrome.
80
Q

Which drugs can cause SIADH?

-mnemonic?

A

Can’t Concentrate Serum Sodium

  • Carbamazepine
  • Cyclophosphamide
  • SSRIs
81
Q

SIADH

  • first step in management?
  • tx:
A
  • 1st step = water restriction
  • demeclocycline = ADH antagonist
  • lithium
  • conivaptan, tolvaptan = ADH antagonists
82
Q

conivaptan, tolvaptan =

A
  • ADH antagonists

- Tx for SIADH

83
Q

Losing pubic hair after pregnancy

A

Sheehan

-need LH for pubic hair.

84
Q

Empty sella syndrome

  • what is it?
  • common in who?
A
  • atrophy or compression of pituitary, often idiopathic, common in obese women.
  • could be due to trauma/congenital reasons.
85
Q

Severe hypoglycemia

-Tx?

A

glucagon injection

86
Q

Most common cause of death in DM?

A

MI

87
Q

DM1

-HSR, which type?

A

-type 4 HSR

88
Q

DM1

-HLA association? if so, which ones?

A
  • HLA-DR3 and 4

- Sxs may be preceded by a viral infection.

89
Q

What does glucose intolerance mean?

A

Unable to take up insulin into cells.

-no insulin.

90
Q

Maturity-onset diabetes of the young (MODY)

associated w/mutation in what?

A

-Glucokinase mutation.

91
Q

Genetic predisposition in DM1 or 2?

A

DM2

  • 90% concordance in idential twins
  • (DM1 has 50% concordance in identical twins).
92
Q

What triggers DKA?

A
  • inc. insulin req due to inc. stress (ie. infection).

- stress triggers symp. nervous system = catecholamines & glucagon.

93
Q

Name some Sxs of DKA.

A
  • Abdominal pain
  • delirium
  • kussmaul respiration
  • fruity breath
  • N/V
  • dehydration
94
Q

DKA

  • total body K?
  • serum K?
A
  • depleted intracellular K = low total body K

- normal/high serum K

95
Q

Why do you get dehydrated in DKA?

A
  • glucosuria causes osmotic diuresis.

- can lead to pre-renal azotemia & elevated BUN.

96
Q

Whipple triad of episodic CNS symptoms:

  • what is it?
  • whats it seen in?
A
  • lethargy, syncope, and diplopia

- insulinoma

97
Q

Episodic hypoglycemia w/mental status changes that

are relieved by glucose.

A

insulinoma

98
Q

Neuroendocrine tumors are positive for what?

A

chromagranin

99
Q

carcinoid tumor can lead to what vitamin deficiency?

A

niacin deficiency

-tryptophan required to make niacin, but your bodys stores are being used to make serotonin instead.

100
Q

carcinoid heart disease

-mnemonic:

A

TIPS: tricuspid insufficiency, pulmonary stenosis.

101
Q

Zollinger Ellison

-mechanism behind steattorhea / malabsorption

A

-too much acid = pancreatic enzymes wont work. They need alkaline environment to operate!

102
Q

Rapid acting insulin

  • mnemonic?
  • use?
A 
There is no LAG w/rapid acting insulin.
Lispro
Aspart
Glulisine
-postprandial glucose control.
103
Q

Long acting insulin

A

Glargine

Detemir

104
Q

Biguanides

  • aka?
  • mech:
  • major side effects?
A
  • Metformin
  • dec. gluconeo, inc. glycolysis, inc. glucose sensitivty.
  • GI upset, lactic acidosis.
  • contraindicated in renal failure
105
Q

Sulfonylureas

  • 1st gen:
  • 2nd gen:
A

First generation:
Tolbutamide
Chlorpropamide

Second generation:
Glyburide
Glimepiride
Glipizide

106
Q

OSUs (sulfonylureas)

-used in DM1 or DM2?

A

DM2

  • requires some islet function, so useless in DM1.
  • closes the K channel (so it mimics normal action of ATP)
107
Q

sulfonylureas

  • side effects
  • 1st gen:
  • 2nd gen:
A

Risk of hypoglycemia inc. in renal failure.

  • First generation: disulfiram-like effects.
  • Second generation: hypoglycemia.

*-can cause weight gain b/c anything that inc. insulin inc. TG storage in adipocytes.

108
Q

Diazoxide and minoxidil mechanism

-opposite of which drugs?

A
  • exactly the opposite as sulfonylureas, which is how they can cause drug induced diabetes (prevent insulin release from beta-cells).
  • potassium channel openers, causing hyperpolarization of cell membranes.
109
Q

Glitazones

  • aka?
  • mech?
  • inc levels of what?
A
  • thiazolidinediones (TZDs)
  • inc. insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.
  • increase levels of adiponectin (inc. insulin sensitivity).
110
Q

Glitazones/TZDs

-side effects?

A

-Weight gain, edema, Hepatotoxicity, heart failure (CHF).

111
Q

Amylin analogs

  • name?
  • mech?
A
  • Pramlintide
  • dec. gastric emptying, dec. glucagon.
  • amylin deposits in islets seen in DM2.
112
Q

GLP-1 analogs

  • name them:
  • mech:
  • notable tox:
A
  • Exenatide, Liraglutide
  • inc. insulin release
  • pancreatitis

*An incretin. Its a small peptide released from small intestine whenever you eat.

113
Q

Which DM drug can lead to pancreatitis?

A

GLP-1 analogs (incretins)

-exenatide, liraglutide.

114
Q

DPP-4 inhibitors (“liptins”)

  • name them
  • mech
  • tox
A
  • Linagliptin, Saxagliptin, Sitagliptin
  • DPP-4 = enzyme that breaks down GLP-1. So by inhibiting DPP-4 you inc. GLP-1.
  • indirectly inc. insulin release.

-tox: Mild urinary or respiratory infections.

115
Q

Propanolol

-addition effect thats useful in thyrotoxicosis besides bocking beta receptors?

A

-also inhibits 5′-deiodinase

116
Q

Propylthiouracil, methimazole

  • which one used in pregnancy?
  • toxicities?
A
  • PTU used in pregnancy, highly protein bound.
  • Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil).
  • Methimazole is a possible teratogen (can cause aplasia cutis).
117
Q

Demeclocycline

-side effects

A
  • Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.
  • member of the tetracycline family. hence the s/e profile.
118
Q

Do glucocorticoids inhibit or stimulate txn factors like

NF-κB?

A

-Inhibit transcription factors such as NF-κB.

  • NF-kB: transcription factor that stimulates cytokine production in the immune response to infectious pathogens.
  • needed for inflammation.
119
Q

Glucocorticoids & peptic ulcers

-how?

A
  • phospholipase A2 inhibitor

- so same mech as NSAID ulcer.

120
Q

Spondyloarthropathies

  • HLA association?
  • HLA association of RA?
A
  • spondylos = HLA-B27

- RA = HLA-DR4

121
Q

Crest Abs =

Systemic sclerosis Abs =

A
  • CREST=anti-centromere

- SS=anti-DNA topoisomerase 1

122
Q

Anti-histone Abs

A

Drug induced lupus

-no renal or CNS involvement

123
Q

Antiphospholipid ab syndrome

  • Sxs
  • PTT time
A
  • hypercoag state, frequent miscarriages

- PTT increased (paradoxically)

124
Q

chronic anemia affect on cardiac output.

A

-chronic anemia inc. CO.

125
Q

Sup. gluteal nerve.

-if you give an injection in which quadrant will you likely damage this nerve?

A

Supero-medial quadrant.

126
Q

PTH

-which pathway

A

inc. cAMP.

127
Q

ankylosing spondylitis

-which murmur can it lead to?

A

-aortic regurg.

128
Q

Probenacid

A
  • inhibits resorption of uric acid in PCT
  • also inhibits secretion of penicillin.

*dont give if possible uric acid stones.

129
Q

febuxostat

A

xanthine oxidase inhibitor

-like allopurinol

Final FA review (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions